Treponema denticola
Treponema denticola | |
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Scientific classification | |
Domain: | Bacteria |
Phylum: | Spirochaetota |
Class: | Spirochaetia |
Order: | Spirochaetales |
Family: | Treponemataceae |
Genus: | Treponema |
Species: | T. denticola
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Binomial name | |
Treponema denticola (ex Flügge 1886) Chan et al. 1993[1]
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Treponema denticola is a
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
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]
- Outer sheath associated peptidases
- Chymotrypsin proteinases
- Trypsin proteinases
- Hemolytic activities
- Hemagglutinating activities
- outer-sheath protein with pore-forming properties
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
Vascular disease
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
- Oral microbiology
- Periodontitis
- List of bacterial vaginosis microbiota
References
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