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Treponema denticola

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A Microbial Biorealm page on the genus Treponema denticola



Higher order taxa

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


Treponema denticola (NCBI: Taxonomy)

Description and significance

Treponema denticola is a gram-negative bacterium from the Spirochetes family that is motile, slender, helically shaped and flexible. The organism consists of periplasmic flagella, which allows for mobility by using a proton motive force to cause thrusting through rotation. The flagellum is wound around a helical protoplasmic cylinder that contains ribosomes, genomic DNA, and other cytoplasmic constituents. (Charon NW, 1992) Its 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 (Seshadri et al., 2004).

Periodontal disease results in inflammation of the gum tissue, bone resorption, 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 (Seshadri et al., 2004). 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

The genome of Treponema denticola strain ATCC 35405 has 2,843,201 base pairs. It is made up of double stranded DNA and a single circular chromosome. The genome is AT rich, with a GC content of 37.9%. (Seshadri et al., 2004) The plasmid sequence, pTS1, has been reported as being related to T. denticola. Since T. denticola is one of the few spirochetes that can be cultured, pTS1 can be used to determine virulence genes for other unculturable spirochetes. By using a shuttle vector and PCR fragments of spirochetes that may be virulent, the function of the proteins that are expressed can be determined. (Bo, 1999)

Cell structure and metabolism

The gram-negative cell envelope of Treponema denticola has an outer membrane that is made up of proteins, phospholipids, and a lipopolysaccharide layer that forms a barrier permeable to hydrophobic substances. Gram negative bacteria also have endotoxin activity and porins, which act as channels through which small molecules can pass through the outer membrane. (Hunt, 2005)

Treponema denticola is anaerobic and cannot survive in the presence of oxygen. It survives at a temperature range that is between freezing and boiling. Thus, since it is a mesophile, it can survive within the oral cavity and is primarily a human pathogen. Most bacteria survive best in neutral pH, but Treponema denticola has the ability to also survive in conditions of pH 6.5 to 8.0. (Hunt, 2005)

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 (Seshadri et al, 2004.). Its spiral shape allows for single arrangement. It is a mobile organism that moves via rapid rotations along its 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.

Typically, anaerobic bacteria produce energy through glycolysis and fermentation (Hunt, 2005). The absence of cytochromes and quinones, molecules that are essential in the electron-transport chain, suggests that T. denticola does not have an electron-transport chain for energy production. Since the TCA cycle is absent in T. denticola, ATP production must be through the fermentation pathway. Furthermore, 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. (Seshadri et al., 2004)


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)

A study found that T. denticola has a 9.6-kb operon made up of 11 genes, including: tap1, flgD, flgE, orf4, motA, motB, fliL, fliM, fliY, orf10 and fliP. Reverse transcription-PCR analysis showed how closely related Treponema denticola and Treponema pallidum are, on the basis that their fla operons are so highly conserved. (Stamm, 1999)


Treponema denticola is a bacterial pathogen that produces endotoxin proteins, which utilize enzymatic activities (Hunt, 2005). It causes periodontal disease and gum inflammation. It's an 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. (Kuramitsu et al, 2005)

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. The gene that encodes T. denticola binding protein, FhbB, was found and characterized by McDowell et al. 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.


Bo Chi, Sarita Chauhan, and Howard Kuramitsu. 1999. “Development of a System for Expressing Heterologous Genes in the Oral Spirochete Treponema denticola and Its Use in Expression of the Treponema pallidum flaA.” Infect Immun. Vol. 67, No. 7, p. 3653–3656.

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.

Charon NW, Greenberg EP, Koopman MB, Limberger RJ. 1992. “Spirochete chemotaxis, motility, and the structure of the spirochetal periplasmic flagella.” Res Microbiol. Vol.143, No.6, p.597-603.

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.

Hunt, D.M. (2005). Bacteriology. Microbiology and Immunology On-line, Hunt, R.C. editor. http://pathmicro.med.sc.edu/mhunt/flu.htm. University of South Carolina School of Medicine, Ch. 3, 4, and 10.

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.

Kuramitsu HK, Chen W, Ikegami A. 2005. “Biofilm formation by the periodontopathic bacteria Treponema denticola and Porphyromonas gingivalis.” J Periodontol. Vol.76, No.11 Suppl, p. 2047-51.

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.

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.

Stamm LV, Bergen HL. 1999. “Molecular characterization of a flagellar (fla) operon in the oral spirochete Treponema denticola ATCC 35405.” FEMS Microbiol Lett. Vol. 179, No. 1, p. 31-6.

Treponema denticola ATCC 35405 project at TIGR. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=genomeprj&cmd=ShowDetailView&TermToSearch=4

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


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