Treponema denticola

A Microbial Biorealm page on the genus Treponema denticola

Classification

Higher order taxa

Cellular organisms; Bacteria; Spirochaetes; Spirochaetes (class); Spirochaetales; Spirochaetaceae; Treponema; Treponema denticola.

Genus

NCBI: Taxonomy [1]

Treponema denticola

Description and significance

Treponema denticola is a motile, slender, helically shaped flexible organism. It is made up of a periplasmic flagella wound around the helical protoplasmic cylinder and encased in an outer sheath. It's habitat is anaerobic and host-associated. It grows at an optimal temperature of 30-42°C, with a pH of 6.5-8.0. It is commonly found in the human oral cavity, specifically in subgingival dental plaque, and it is often associated with periodontal disease. Periodontal disease results in inflammation of the gum tissue, bone resorbtion, and subsequent tooth loss. Periodontal disease has now become a major concern in dentistry and 80% of adults in the USA are estimated to have had periodontal disease at some point in their lives. The complete genome of T. denticola strain 35405 was sequenced by using the random shotgun method described for genomes sequenced by The Institute for Genomic Research and it was designated as the type strain by Chan et al.

Genome structure

Treponema denticola ATCC 35405 has a complete genome. It is made up of dsDNA and 1 chromosome. It is circular and the length is 2,843,201 nucleotides. The GC content is 37%. It has 2838 genes. Replicon Type: chromosome.

A plasmid sequence, pTS1, has been reported in association with T.denticola.

Cell structure and metabolism

The genome of T. denticola has shown to be involved in cell to cell signaling, as well as cell protection from external stressors such as oxidation and osmosis. It's spiral shape allows for single arrangement. It is a mobile organism that moves via rapid rotations along it's vertical axis, and rotations along the helical path allow for body flexion. A distinguishable characteristic of T. denticola is the flagella found in the space between the plasma membrane and the outer membrane (periplasmic space), which wraps around the protoplasmic cylinder.

T. denticola has a variety of mechanisms to compensate for osmosis, oxidation and many other external stressors. Studies have shown T. denticola to possess enzymes such as NADH peroxidase, NADH oxidase and superoxide dismutase.

In contrast to other spirochetes, T. denticola possesses enzymes that are essential for the synthesis of glycogen. The existence of such enzymes can be advantageous during starvation situations.

T. denticola is comprised of amino acid and peptide uptake mechanisms, including eight ABC-tyep peptide uptake systems.

The two general pathways of ATP synthesis are Glycolysis through the TCA cycle, and sugar fermentation. Since glycolysis and the TCA cycle are absent in T. denticola, ATP production must be through the sugar fermentation pathway. Furthermore, the absence of cytochromes and quinones, cells that are essential in the electron-transport chain, suggests that T. denticola does not have an electron-transport chain for energy production.

Ecology

It has been found that in order to begin the onset of periodontal disease, T. denticola must interact with other oral bacteria, such as Porphyromonas gingivalis. This interaction creates a biofilm, which is a community of bacteria with inert surfaces that allow further bacteria to colonize the oral cavity without being affected by saliva flow.(Vesey et al., 2004)

T. denticola has been shown to adhere to various cell types and basement membranes via binding to fibronectin, collagen, laminin, fibrinogen, and other substrates. Additionally, because T. denticola is a late colonizer during plaque biofilm formation, adhesion to other oral bacteria is critical.(Vesey et al., 2004)

Pathology

Treponema denticola is a bacterial pathogen. It causes periodontal disease and gum inflammation. It's a infection caused by several types of microorganisms of the gingiva that can lead to severe effects including refractory periodontitis and acute necrotizing gingivitis, resulting in bone resorption and tooth loss. This organism causes disease by aggregating in subgingival plaque with Porphyromonas gingivalis and it uses several mechanisms in order to survive harsh conditions, such as oral biofilms.

Application to Biotechnology

Treponema denticola is resistant to the harsh environment produced by beta-defensins. Beta-defensins are antimicrobrial peptides with activity to destroy microbes and periodontal pathogens. Beta-defensins are produced by the oral epithelium, tongue, and salivary glands, and are used as an immune response during inflammation. Treponema denticola's ability to survive the effects of beta-defensins is a characteristic that can provide insight into possible treatments to break down such organisms.(Brissette et al., 2007)

Current Research

Prior research has shown that polymorphism of Interleuken-1 (IL-1) influences the progression of periodontal disease. A study done by Kowalski et al. aimed to measure the amount of microbacteria in patients with positive and negative genotypes. The results were that, though both positive and negative genotype patients had the same bacterial pathogens in the periodontal pockets, they were greater in number in the positive genotype group. T. denticola was included in the group of microbacterial pathogens analyzed.

A study done by Colombo et al. aimed at identifying which bacterial microbes play an integral role in the onset of periodontal disease. It was found that those with periodontitis exhibited more bacteria per cell than the controls. Furthermore, T. forsythia and T. denticola were significantly more apparent in periodontal pockets than in the healthy sulci.

Further research needs to be conducted on the pathogenesis of T. denticola. One study, by McDowell et al., attempted to do this by identifying T. The gene that encodes T. denticola binding protein, FhbB, was found and characterized. The characterization of this protein will be vital in the understanding the pathogenesis of T. denticola and how exactly it binds and grows during periodontal disease.

References

1)Rekha Seshadri, Garry S. A. Myers, Hervé Tettelin, Jonathan A. Eisen, John F. Heidelberg, Robert J. Dodson, Tanja M. Davidsen, Robert T. DeBoy, Derrick E. Fouts, Dan H. Haft, Jeremy Selengut, Qinghu Ren, Lauren M. Brinkac, Ramana Madupu, Jamie Kolonay, Scott A. Durkin, Sean C. Daugherty, Jyoti Shetty, Alla Shvartsbeyn, Elizabeth Gebregeorgis, Keita Geer, Getahun Tsegaye, Joel Malek, Bola Ayodeji, Sofiya Shatsman, Michael P. McLeod, David Šmajs, Jerrilyn K. Howell, Sangita Pal, Anita Amin, Pankaj Vashisth, Thomas Z. McNeill, Qin Xiang, Erica Sodergren, Ernesto Baca, George M. Weinstock, Steven J. Norris, Claire M. Fraser, and Ian T. Paulsen. 2004. “Comparison of the genome of the oral pathogen Treponema denticola with other spirochete genomes.” “Proc Natl Acad Sci U S A”. Vol. 101, No. 15

2) Catherine A. Brissette1, Sheila A. Lukehart. 2007. "Mechanisms of Decreased Susceptibility to ß-Defensins by Treponema denticola." "Infection and Immunity". Vol. 75, No. 5, p. 2307-2315.

3)Colombo AV, da Silva CM, Haffajee A, Colombo AP. 2007 June. "Identification of intracellular oral species within human crevicular epithelial cells from subjects with chronic periodontitis by fluorescence in situ hybridization." "J Periodontal Res". Vol. 42, No. 3, p. 236-43.

4)Kowalski J, Gorska R, Dragan M, Kozak I. 2006. "Clinical state of the patients with periodontitis, IL-1 polymorphism and pathogens in periodontal pocket--is there a link? (An introductory report)." Adv Med Sci. Vol. 51, Supp l1, p. 9-12.

5)McDowell JV, Frederick J, Stamm L, Marconi RT.2007 Feb. "Identification of the gene encoding the FhbB protein of Treponema denticola, a highly unique factor H-like protein 1 binding protein." "Infect Immun". Vol.75, No.2, p.1050-4.

Edited by Neena Patel, student of Rachel Larsen and Kit Pogliano.