Porphyromonas gingivalis

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A Microbial Biorealm page on the genus Porphyromonas gingivalis

[edit] Classification

[edit] Higher order taxa

Bacteria; Bacteroidetes/Chlorobi group; Bacteroidetes; Bacteroides (class); Bacteroidales; Porphyromonadaceae

[edit] Genus

Porphyromonas gingivalis

NCBI: Taxonomy

[edit] Description and significance

Porphyromonas gingivalis is gram-negative and has black spots. It resides in mouth below the gingival surface. It is one of the common pathogens in early onset periodontitis (inflammation of the gingiva). This microbe works with other bacteria to create a biofilm in the subgingival layer that replaces the existing gram-positive, facultative bacteria with gram-negative anaerobic bacteria, eliciting an inflammatory response that results in the gums detaching from the teeth. It is usually found with ,Treptonema denticola and Bacteroides forsythus.

[edit] Genome structure

Currently, 2,015 Genes have been identified with 23,43,479 nucleotides. It has a circular genome with its oriC (origin of replication) lying between the genes dnaA and PG1949. It has a G+C content of 49%.
The genome contains many genes that do not require a rho factor to terminate. [1]

[edit] Cell structure and metabolism

P. gingivalis is an anaerobic, gram-negative bacteria that is shaped as a rod. It uses fimbriae as an adhesive mechanism to stick to the gum layer of the mouth. Fimbriae also act as pathogens that are identified by the immune system.

[edit] Iron Transport

P. gingivalis has no known siderophores, so to acquire iron, it uses hemin as a mechanism to transport iron. These accumulations of hemin give the black pigmentation observed. It uses an ABC Transporter to import the hemin iron complex into the cell.

[edit] Metabolism

P. gingivalis can undergo the following metabolic processes [2]:

[edit] Carbohydrate Metabolism

Glycolysis / Gluconeogenesis
Citrate cycle (TCA cycle)
Pentose phosphate cycle
Pentose and glucuronate interconversions
Fructose and mannose metabolism
Galactose metabolism
Ascorbate and aldarate metabolism
Pyruvate metabolism
Glyoxylate and dicarboxylate metabolism
Propanoate metabolism
Butanoate metabolism
C5-Branched dibasic acid metabolism

[edit] Energy Metabolism

Oxidative phosphorylation
ATP synthase
Methane metabolism
Carbon fixation
Reductive carboxylate cycle (CO2 fixation)
Nitrogen metabolism
Sulfur metabolism

[edit] Lipid Metabolism

Fatty acid biosynthesis
Fatty acid metabolism
Synthesis and degradation of ketone bodies
Sterol biosynthesis
Bile acid biosynthesis
C21-Steroid hormone metabolism
Androgen and estrogen metabolism

[edit] Nucleotide Metabolism

Purine metabolism
Pyrimidine metabolism
Nucleotide sugars metabolism

[edit] Amino Acid Metabolism

Glutamate metabolism
Alanine and aspartate metabolism
Glycine, serine and threonine metabolism
Methionine metabolism
Cysteine metabolism
Valine, leucine and isoleucine degradation
Valine, leucine and isoleucine biosynthesis
Lysine biosynthesis
Lysine degradation
Arginine and proline metabolism
Histidine metabolism
Tyrosine metabolism
Phenylalanine metabolism
Tryptophan metabolism
Phenylalanine, tyrosine and tryptophan biosynthesis
Urea cycle and metabolism of amino groups

[edit] Metabolism of Other Amino Acids

beta-Alanine metabolism
Taurine and hypotaurine metabolism
Aminophosphonate metabolism
Selenoamino acid metabolism
Cyanoamino acid metabolism
D-Glutamine and D-glutamate metabolism
D-Arginine and D-ornithine metabolism
D-Alanine metabolism
Glutathione metabolism

[edit] Metabolism of Complex Carbohydrates

Starch and sucrose metabolism
Biosynthesis and degradation of glycoprotein
Aminosugars metabolism
Lipopolysaccharide biosynthesis
Peptideglycan biosynthesis
Glycosaminoglycan degradation

[edit] Metabolism of Complex Lipids

Glycerolipid metabolism
Inositol phosphate metabolism
Sphingophospholipid biosynthesis
Phospholipid degradation
Sphingoglycolipid metabolism
Prostaglandin and leukotriene metabolism

[edit] Metabolism of Cofactors and Vitamins

Thiamine metabolism
Riboflavin metabolism
Vitamin B6 metabolism
Nicotinate and nicotinamide metabolism
Pantothenate and CoA biosynthesis
Biotin metabolism
Folate biosynthesis
One carbon pool by folate
Retinol metabolism
Porphyrin and chlorophyll metabolism
Ubiquinone biosynthesis

[edit] Ecology

P. gingivalis mainly inhabits the oral cavities of mammals. It has been found that it usually inhabits similar niches other oral pathogens inhabit, such as Treptonema denticola and Bacteroides forsythus. [3] Whether it works in symbiosis with these other organisms is still under speculation.

[edit] Pathology

P. gingivalis is one of the bacteria that is known to cause gingivitis (inflammation of the gingiva) and periodontitis (inflammation of the periodontium or other supporting tissues). If it is not treated, gingivitis can escalate into Acute Necrotizing Ulcerative Gingivitis (ANUG).

Gingivitis starts out with a bacterial accumulation of many gram-negative anaerobic bacteria (including P. gingivalis and Actinobacillus actinomycetemcomitans)on the gum line which if not cleaned build up. With time, they begin to form a special biofilm on the tooth called plaque. Plaque that is left untreated then form lesions around the tooth that go beneath the gum layer. P gingivalis then begins to express its proteolytic enzymes which are normally used for Cysteine and Arginine metabolism (usually collagenolytic enzymes although trypsin-like and glycylpropyl peptidases have also been identified to contribute to protein metabolism). Its main target is the tooth ligaments that connect the tooth to the gum/bone. As the lesion begins to grow, more ligaments are destroyed eventually leading to the loosening/separation of the tooth from the jaw.[4]
Periodontitis is also associated with atherosclerosis, however as of now, no causal relationship either way has been proven. It is known however P. gingivalis can accelerate the transformation of macrophages into foam cells. [5]

[edit] Immunological Activities

Initial deposition of fibrin and collagenolytic activity elicits an innate immune response, causing neutrophils to migrate to the plaque sites. As lesions begin to form, lymphocytes begin to deposit into the lesions along with monocytes and plasma cells. As lesions become chronic, the humoral immune system activates, sending plasma cells and B lymphocytes to the lesion sites. [6] The T-Cell mediated response has been found to be generally lower in comparison to other infectious responses. Although CD8+ T-Cells may help in removing damaged host cells, they do not actively fight against peridontal tissue destruction. [7]

Some identified virulence factors in P. gingivalis can be found here.

[edit] Symptoms of Gingivitis

[8]

Swelling, redness, and pain in the gums
Bad Breath
Gums fail to have structure
Inflammation of gums

[edit] Current Research

Currently, scientists are trying to find exactly how the symbiosis among the bacterial populations within the mouth works, specifically between P. gingivalis and Actinobacillus actinomycetemcomitans as they are the major causes of gingivitis. Their specific aims include to see what components are shuttled between the bacteria as it has already been proven that neither bacterial species can survive without the other. [9]

Also more studies are focusing on the fimbriae, specifically finding ways to inhibit the minor fimbriae production as that would prevent the formation of a biofilm on the tooth. [10]

Another major area of research is finding out how current methods to destroy these pathogens work, such as ammonium nitrate. Even though people have used solutions like these for a while now, the exact mechanism for how they are cytotoxic is unknown. [11]