Treponema denticola

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Treponema denticola
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Bacteria
Phylum: Spirochaetota
Class: Spirochaetia
Order: Spirochaetales
Family: Treponemataceae
Genus: Treponema
Species:
T. denticola
Binomial name
Treponema denticola
(ex Flügge 1886) Chan et al. 1993 [1]

Treponema denticola is a Gram-negative, obligate anaerobic, motile and highly proteolytic spirochete bacterium. It is one of four species of oral spirochetes to be reliably cultured, the others being Treponema pectinovorum, Treponema socranskii and Treponema vincentii [2] . T. denticola dwells in a complex and diverse microbial community within the oral cavity and is highly specialized to survive in this environment. T. denticola is associated with the incidence and severity of human periodontal disease. Treponema denticola is one of three bacteria that form the Red Complex, the other two being Porphyromonas gingivalis and Tannerella forsythia . Together they form the major virulent pathogens that cause chronic periodontitis. [3] Having elevated T. denticola levels in the mouth is considered one of the main etiological agents of periodontitis. [4] [5] T. denticola is related to the syphilis-causing obligate human pathogen, Treponema pallidum subsp. pallidum. It has also been isolated from women with bacterial vaginosis. [6]

Contents

Genome

The first genome of T. denticola to be sequenced was strain 35405 which was initially isolated and designated as the type strain by Chan et al. [7] The 2,843,201-bp genome sequence encodes 2,786􏴲 open reading frames (ORFs) as well a 6 rRNAs and 44 tRNAs. This is in stark contrast to the minimal genome of Treponema pallidum which encodes only 1,040 ORFs. [8]

Cell structure

The native cellular architecture of the bacterial cell was revealed using cryo-electron tomography, a technique observing intact plunge-frozen cells. [9] Tightly organized bundles of periplasmic flagella were observed in the periplasm, a characteristic of spirochetes. The presence of the periplasmic flagella is widely regarded as being responsible for the microorganism's ability to rotate and flex, in addition to its translational movement. [2] Spirochetes, including Treponema denticola , are therefore able to navigate through particularly viscous environments, unlike that of other prokaryotes. [2]

The tapering of the cell ends, conserved between cells, encompass a patella-shaped structure observed in the periplasm at the cell tip. This structure might be involved in the polar attachment of the cells. [10] Cytoplasmic filaments, a bacterial intermediate-like filaments composed of the protein CfpA, are adjacent to the inner membrane and run parallel to the tightly organized flagellar filaments. [9] [11] Those cytoplasmic filaments are critical for pathogenicity, directly or indirectly as they are also involved in chromosome structure, segregation, or the cell division processes. [12] [13] The absence of either flagella or cytoplasmic filaments in deficient mutant increase the mouse peritoneal macrophages in vitro uptake. [14]

Adherence and cytotoxicity

The main site for T. denticola habitation in the oral cavity is the gingival crevice. These spirochetes attach to proteins (including fibronectin and collagen) of local gingival fibroblasts, binding to their plasma membrane. A 53-kDa surface protein on T. denticola is responsible for transporting its components into the host cell, exhibiting a cytotoxic effect. Accumulation of T. denticola in this manner facilitates the disease-causing process, including membrane blebbing and red blood cell lysis. [2]

Role in disease

Periodontal disease

Periodontal disease is a type of gum disease caused by the accumulation of plaque on the teeth due to poor oral hygiene. Plaque is a sticky substance that contains bacteria which can harden into a substance called calculus, irritating the gums. [15]

[16] Treponema denticola, a subgingival oral spirochete has been associated with many periodontal disease conditions such as: the early stage of periodontitis, acute pericoronitis (infection under the gum tissue covering a partially erupted tooth)3, as well as necrotising ulcerative gingivitis (severe inflammation of the gum more common in immunocompromised patients). It relates to lesions limited to gingival tissue. [17]

Clinical evidence and research shows that periodontal pockets contain large numbers of treponema denticola together with other proteolytic gram negative bacteria, playing an important role in the development of periodontal disease. The toxic products of these bacteria, especially treponema denticola may damage the surface lining periodontal cells making them more prone to damage as well as lysis. Treponema denticola attaches to fibroblasts and epithelial cells as well as to extracellular matrix components which are found in periodontal tissues and release its own bacterial contents. The bacterial components are:[ citation needed ]

A number of studies have observed an increase of T. denticola in patients with orthodontic appliances, particularly the fixed type. [18]

Oral cancer

Treponema denticola is a potential etiological bacterial agent for oral cancer. [19] It encourages oncogenesis (process in which healthy cells become cancer cells) and therefore the progression of oral cancer through chronic inflammation advancing invasiveness of the cancer cells. This results in the ceasing of cell apoptosis (inhibition of controlled cell death – a safety mechanism within cells to stop more damage from occurring), resulting in rapid growth and multiplication of cancer cells. This suppresses the immune system stopping the body from recognising the cancerous cells and as a result more cancer-promoting substances are produced. [19]  The presence of T. denticola along with other periodontal pathogens and bacterial diversity within the oral cavity are important factors contributing to cancerous cells (including precancerous gastric lesions). [20]

Vascular disease

Atherosclerotic vascular disease is chronic inflammatory disease of large arteries distinguished by invasion, proliferation and accumulation of cells from arterial smooth muscle cells, and the circulating blood in the intimal layer with deposition of connective tissue and lipids, if left to get worse atherosclerotic vascular disease can result in cardiovascular disease. Cardiovascular disease (including angina, heart attack, arrhythmias, heart failure, strokes) is the leading cause of death globally.  [ citation needed ]

Substantial evidence between inflammation from infectious agents and development of atherosclerosis – periodontal pathogens prominent contenders due to chronic inflammation related with periodontal disease.[ citation needed ]

Treponema denticola bacteria can penetrate gingival tissues and circulate through blood vessels, with opportunity to invade the heart and cardiovascular epithelium in medium to large arteries – including aorta, coronary and carotid arteries. [21]

Pancreatic cancer

It has been recognised that there is an association between oral and intestinal cancer related deaths and chronic periodontitis. This is based on the high amounts of tumor suppressor gene p53 mutations and k-ras arginine mutations found in patients with pancreatic cancer. Peptidylarginine deiminases from oral bacteria are thought to be responsible for these mutations. This means that there could be a causative link between oral bacteria, particularly the red complex, and pancreatic cancer. [3]

See also

Related Research Articles

<i>Treponema pallidum</i> Species of bacterium

Treponema pallidum, formerly known as Spirochaeta pallida, is a spirochaete bacterium with various subspecies that cause the diseases syphilis, bejel, and yaws. It is transmitted only among humans. It is a helically coiled microorganism usually 6–15 μm long and 0.1–0.2 μm wide. T. pallidum's lack of either a tricarboxylic acid cycle or oxidative phosphorylation results in minimal metabolic activity. The treponemes have a cytoplasmic and an outer membrane. Using light microscopy, treponemes are visible only by using dark-field illumination. T. pallidum consists of three subspecies, T. p. pallidum, T. p. endemicum, and T. p. pertenue, each of which has a distinct associated disease.

<span class="mw-page-title-main">Periodontal disease</span> Medical condition

Periodontal disease, also known as gum disease, is a set of inflammatory conditions affecting the tissues surrounding the teeth. In its early stage, called gingivitis, the gums become swollen and red and may bleed. It is considered the main cause of tooth loss for adults worldwide. In its more serious form, called periodontitis, the gums can pull away from the tooth, bone can be lost, and the teeth may loosen or fall out. Bad breath may also occur.

<span class="mw-page-title-main">Calculus (dental)</span> Form of hardened dental plaque

In dentistry, calculus or tartar is a form of hardened dental plaque. It is caused by precipitation of minerals from saliva and gingival crevicular fluid (GCF) in plaque on the teeth. This process of precipitation kills the bacterial cells within dental plaque, but the rough and hardened surface that is formed provides an ideal surface for further plaque formation. This leads to calculus buildup, which compromises the health of the gingiva (gums). Calculus can form both along the gumline, where it is referred to as supragingival, and within the narrow sulcus that exists between the teeth and the gingiva, where it is referred to as subgingival.

Periodontology or periodontics is the specialty of dentistry that studies supporting structures of teeth, as well as diseases and conditions that affect them. The supporting tissues are known as the periodontium, which includes the gingiva (gums), alveolar bone, cementum, and the periodontal ligament. A periodontist is a dentist that specializes in the prevention, diagnosis and treatment of periodontal disease and in the placement of dental implants.

Dental plaque is a biofilm of microorganisms that grows on surfaces within the mouth. It is a sticky colorless deposit at first, but when it forms tartar, it is often brown or pale yellow. It is commonly found between the teeth, on the front of teeth, behind teeth, on chewing surfaces, along the gumline (supragingival), or below the gumline cervical margins (subgingival). Dental plaque is also known as microbial plaque, oral biofilm, dental biofilm, dental plaque biofilm or bacterial plaque biofilm. Bacterial plaque is one of the major causes for dental decay and gum disease.

Dysbiosis is characterized by a disruption to the microbiome resulting in an imbalance in the microbiota, changes in their functional composition and metabolic activities, or a shift in their local distribution. For example, a part of the human microbiota such as the skin flora, gut flora, or vaginal flora, can become deranged, with normally dominating species underrepresented and normally outcompeted or contained species increasing to fill the void. Dysbiosis is most commonly reported as a condition in the gastrointestinal tract.

Fusobacterium nucleatum is a Gram-negative, anaerobic oral bacterium, commensal to the human oral cavity, that plays a role in periodontal disease. This organism is commonly recovered from different monocultured microbial and mixed infections in humans and animals. In health and disease, it is a key component of periodontal plaque due to its abundance and its ability to coaggregate with other bacteria species in the oral cavity.

Porphyromonas gingivalis belongs to the phylum Bacteroidota and is a nonmotile, Gram-negative, rod-shaped, anaerobic, pathogenic bacterium. It forms black colonies on blood agar.

Aggregatibacter actinomycetemcomitans is a Gram-negative, facultative anaerobe, nonmotile bacterium that is often found in association with localized aggressive periodontitis, a severe infection of the periodontium. It is also suspected to be involved in chronic periodontitis. Less frequently, A. actinomycetemcomitans is associated with nonoral infections such as endocarditis. Its role in aggressive periodontitis was first discovered by Danish-born periodontist Jørgen Slots, a professor of dentistry and microbiology at the University of Southern California School of Dentistry.

<span class="mw-page-title-main">Scaling and root planing</span> Dental procedure

Scaling and root planing, also known as conventional periodontal therapy, non-surgical periodontal therapy or deep cleaning, is a procedure involving removal of dental plaque and calculus and then smoothing, or planing, of the (exposed) surfaces of the roots, removing cementum or dentine that is impregnated with calculus, toxins, or microorganisms, the agents that cause inflammation. It is a part of non-surgical periodontal therapy. This helps to establish a periodontium that is in remission of periodontal disease. Periodontal scalers and periodontal curettes are some of the tools involved.

<span class="mw-page-title-main">Oral microbiology</span>

Oral microbiology is the study of the microorganisms (microbiota) of the oral cavity and their interactions between oral microorganisms or with the host. The environment present in the human mouth is suited to the growth of characteristic microorganisms found there. It provides a source of water and nutrients, as well as a moderate temperature. 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.

<span class="mw-page-title-main">Prokaryotic cytoskeleton</span> Structural filaments in prokaryotes

The prokaryotic cytoskeleton is the collective name for all structural filaments in prokaryotes. It was once thought that prokaryotic cells did not possess cytoskeletons, but advances in visualization technology and structure determination led to the discovery of filaments in these cells in the early 1990s. Not only have analogues for all major cytoskeletal proteins in eukaryotes been found in prokaryotes, cytoskeletal proteins with no known eukaryotic homologues have also been discovered. Cytoskeletal elements play essential roles in cell division, protection, shape determination, and polarity determination in various prokaryotes.

<span class="mw-page-title-main">Gingivitis</span> Inflammation of the gums

Gingivitis is a non-destructive disease that causes inflammation of the gums. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms that is attached to tooth surfaces, termed plaque-induced gingivitis. Most forms of gingivitis are plaque-induced.

<i>Porphyromonas</i> Genus of bacteria

Porphyromonas is a Gram-negative, non-spore-forming, obligately anaerobic and non-motile genus from the family Porphyromonadaceae. There were 16 different Porphyromonas species documented as of 2015, which reside in both animal and human reservoirs. It was discovered more recently that Porphyromonas also exist in the environment, albeit to a lesser extent. This genus is notably implicated in the modulation of oral cavity, respiratory tract, and gastrointestinal tract disease states. It is suggested that Porphyromonas either operate as benign bacteria pertinent to host immunity or are potential pathobionts that opportunistically provoke diseased states when homeostasis is disrupted. Despite its characterization not being fully elucidated due to sparse research, various studies report the prevalence of this genus at 58.7% in healthy states compared with 41.3% in diseased states.

Tannerella forsythia is an anaerobic, Gram-negative bacterial species of the Bacteroidota phylum. It has been implicated in periodontal diseases and is a member of the red complex of periodontal pathogens. T. forsythia was previously named Bacteroides forsythus and Tannerella forsythensis.

Chronic periodontitis is one of the seven categories of periodontitis as defined by the American Academy of Periodontology 1999 classification system. Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues that is caused by the accumulation of profuse amounts of dental plaque. Periodontitis initially begins as gingivitis and can progress onto chronic and subsequent aggressive periodontitis according to the 1999 classification.

Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis as defined by the 1999 classification system:

  1. Localized aggressive periodontitis (LAP)
  2. Generalized aggressive periodontitis (GAP)

Well studied Periodontal pathogens are bacteria that have been shown to significantly contribute to periodontitis.

Treponema socranskii was isolated from gum swabs of people with periodontitis and clinically-induced periodontitis. It is a motile, helically coiled, obligate anaerobe that grows best at 37 °C, and is a novel member of its genus because of its ability to ferment molecules that other Treponema species cannot. T. socranskii’s growth is positively correlated with gingival inflammation, which indicates that it is a leading cause of gingivitis and periodontitis.

References

  1. ↑ Parte AC. "Treponema". LPSN .
  2. 1 2 3 4 Chan EC, McLaughlin R (February 2000). "Taxonomy and virulence of oral spirochetes". Oral Microbiology and Immunology. 15 (1): 1–9. doi:10.1034/j.1399-302x.2000.150101.x. PMID   11155157.
  3. 1 2 Öğrendik M (March 2017). "Periodontal Pathogens in the Etiology of Pancreatic Cancer". Gastrointestinal Tumors. 3 (3–4): 125–127. doi:10.1159/000452708. PMC   5465713 . PMID   28611978.
  4. ↑ Marie-Claude Jobin; Mohsen Amin; Richard P. Ellen (2008). "Chapter 8 - The Molecular Biology of the Survival and Virulence of Treponema denticola". In Anthony H. Rogers (ed.). Molecular Oral Microbiology. Caister Academic Press. p. 177. ISBN   978-1-904455-24-0.
  5. ↑ Simonson LG, Goodman CH, Bial JJ, Morton HE (April 1988). "Quantitative relationship of Treponema denticola to severity of periodontal disease". Infection and Immunity. 56 (4): 726–8. doi:10.1128/IAI.56.4.726-728.1988. PMC   259361 . PMID   3346072.
  6. ↑ Africa CW, Nel J, Stemmet M (July 2014). "Anaerobes and bacterial vaginosis in pregnancy: virulence factors contributing to vaginal colonisation". International Journal of Environmental Research and Public Health. 11 (7): 6979–7000. doi: 10.3390/ijerph110706979 . PMC   4113856 . PMID   25014248.
  7. ↑ Chan EC, Siboo R, Keng T, Psarra N, Hurley R, Cheng SL, Iugovaz I (April 1993). "Treponema denticola (ex Brumpt 1925) sp. nov., nom. rev., and identification of new spirochete isolates from periodontal pockets". International Journal of Systematic Bacteriology. 43 (2): 196–203. doi: 10.1099/00207713-43-2-196 . PMID   8494734.
  8. ↑ Seshadri R, Myers GS, Tettelin H, Eisen JA, Heidelberg JF, Dodson RJ, et al. (April 2004). "Comparison of the genome of the oral pathogen Treponema denticola with other spirochete genomes". Proceedings of the National Academy of Sciences of the United States of America. 101 (15): 5646–51. Bibcode:2004PNAS..101.5646S. doi: 10.1073/pnas.0307639101 . PMC   397461 . PMID   15064399.
  9. 1 2 Izard J, Hsieh CE, Limberger RJ, Mannella CA, Marko M (July 2008). "Native cellular architecture of Treponema denticola revealed by cryo-electron tomography". Journal of Structural Biology. 163 (1): 10–7. doi:10.1016/j.jsb.2008.03.009. PMC   2519799 . PMID   18468917.
  10. ↑ Ellen RP, Dawson JR, Yang PF (April 1994). "Treponema denticola as a model for polar adhesion and cytopathogenicity of spirochetes". Trends in Microbiology. 2 (4): 114–9. doi:10.1016/0966-842x(94)90597-5. PMID   8012753.
  11. ↑ Izard J, McEwen BF, Barnard RM, Portuese T, Samsonoff WA, Limberger RJ (February 2004). "Tomographic reconstruction of treponemal cytoplasmic filaments reveals novel bridging and anchoring components". Molecular Microbiology. 51 (3): 609–18. doi: 10.1046/j.1365-2958.2003.03864.x . PMID   14731266.
  12. ↑ Izard J, Sasaki H, Kent R (2012). "Pathogenicity of Treponema denticola Wild-Type and Mutant Strain Tested by an Active Mode of Periodontal Infection Using Microinjection". International Journal of Dentistry. 2012: 549169. doi: 10.1155/2012/549169 . PMC   3398590 . PMID   22829826.
  13. ↑ Izard J, Samsonoff WA, Limberger RJ (February 2001). "Cytoplasmic filament-deficient mutant of Treponema denticola has pleiotropic defects". Journal of Bacteriology. 183 (3): 1078–84. CiteSeerX   10.1.1.488.5178 . doi:10.1128/JB.183.3.1078-1084.2001. PMC   94976 . PMID   11208807.
  14. ↑ Gaibani P, Vocale C, Ambretti S, Cavrini F, Izard J, Miragliotta L, et al. (May 2010). "Killing of Treponema denticola by mouse peritoneal macrophages". Journal of Dental Research. 89 (5): 521–6. doi:10.1177/0022034510363105. PMC   2868591 . PMID   20200417.
  15. ↑ "Periodontal Care". SDCEP. Retrieved 2019-12-11.
  16. ↑ Sela MN (2001). "Role of Treponema denticola in periodontal diseases". Critical Reviews in Oral Biology and Medicine. 12 (5): 399–413. doi:10.1177/10454411010120050301. PMID   12002822.
  17. ↑ "Management of acute dental problems. Guidance for healthcare professionals" (PDF).
  18. ↑ Lucchese A, Bondemark L, Marcolina M, Manuelli M (January 2018). "Changes in oral microbiota due to orthodontic appliances: a systematic review". Journal of Oral Microbiology. 10 (1): 1476645. doi:10.1080/20002297.2018.1476645. PMC   6032020 . PMID   29988826.
  19. 1 2 Nieminen MT, Listyarifah D, Hagström J, Haglund C, Grenier D, Nordström D, et al. (February 2018). "Treponema denticola chymotrypsin-like proteinase may contribute to orodigestive carcinogenesis through immunomodulation". British Journal of Cancer. 118 (3): 428–434. doi:10.1038/bjc.2017.409. PMC   5808028 . PMID   29149107.
  20. ↑ Zhang WL, Wang SS, Wang HF, Tang YJ, Tang YL, Liang XH (November 2019). "Who is who in oral cancer?". Experimental Cell Research. 384 (2): 111634. doi:10.1016/j.yexcr.2019.111634. PMID   31541617. S2CID   202718495.
  21. ↑ Chukkapalli SS, Rivera MF, Velsko IM, Lee JY, Chen H, Zheng D, et al. (May 2014). "Invasion of oral and aortic tissues by oral spirochete Treponema denticola in ApoE(-/-) mice causally links periodontal disease and atherosclerosis". Infection and Immunity. 82 (5): 1959–67. doi:10.1128/IAI.01511-14. PMC   3993427 . PMID   24566627.
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