Tannerella forsythia is an anaerobic, Gram-negative bacterium found in the human oral cavity. It is recognized as a major contributor to the development of advanced gum disease, which represents one of the most common chronic infections globally. The bacterium’s presence and activity are closely linked to the severity of this oral condition.
Characteristics and Habitat
The bacterium Tannerella forsythia is a fastidious organism with specific growth requirements. It is a non-motile, spindle-shaped rod that thrives in the oxygen-deprived environment beneath the gum line in a dental plaque biofilm. This organism is recognized as one of the three primary members of the “red complex,” a grouping of bacteria strongly associated with severe periodontitis, alongside Porphyromonas gingivalis and Treponema denticola.
To survive and colonize the subgingival space, T. forsythia often relies on co-aggregation with other bacterial species, such as Fusobacterium nucleatum. A unique feature of its structure is a crystalline cell surface layer, known as the S-layer, which fully covers the bacterial cell. This S-layer is composed of two glycoproteins modified by a complex O-glycosylation system, which aids the bacterium in host interaction and evasion of the immune system.
Pathogenesis in Periodontal Disease
Tannerella forsythia plays a direct role in the destruction of the tissues supporting the teeth through the release of potent virulence factors. The bacterium produces various proteases, enzymes that break down host proteins. These destructive enzymes, including KLIKK proteases and PrtH, are capable of degrading structural components like collagen, gelatine, and elastin, which form the connective tissue of the gums and periodontal ligament.
The BspA surface layer protein contributes to the disease process by facilitating the bacterium’s adherence to and invasion of gum epithelial cells. It also mediates binding to components of the extracellular matrix. Furthermore, T. forsythia possesses a sialidase enzyme that cleaves sialic acid from host glycoproteins, allowing the bacterium to utilize these molecules as a nutrient source.
The presence of the bacterium and its toxins triggers a persistent inflammatory response in the host tissues. This inflammation ultimately leads to the recession of gum tissue and the breakdown of the alveolar bone that anchors the teeth. Studies in animal models have shown that the BspA protein is directly involved in causing alveolar bone loss, highlighting its significance in the progression of periodontitis.
Systemic Health Implications
The impact of Tannerella forsythia is not confined to the mouth; its presence is linked to several conditions outside the oral cavity. This systemic connection involves the translocation of the bacterium or its toxins into the bloodstream from the inflamed periodontal pockets. This process contributes to a state of low-grade, chronic systemic inflammation throughout the body.
One of the most researched connections is with cardiovascular disease, particularly atherosclerosis. T. forsythia has been detected within atherosclerotic plaques, and its virulence factor BspA has been shown to induce the formation of foam cells, which are precursor cells for atherosclerotic lesions. The presence of T. forsythia is also associated with elevated levels of total cholesterol and atherogenic low-density lipoprotein (LDL) in periodontitis patients.
The bacterium has also been associated with other systemic health concerns, including type 2 diabetes and adverse pregnancy outcomes. The chronic inflammation driven by the infection can impair the body’s ability to regulate blood sugar, contributing to diabetes progression. T. forsythia has also been isolated from women with bacterial vaginosis and linked to an increased risk of esophageal cancer.
Identification and Therapeutic Approaches
Identifying Tannerella forsythia is crucial for diagnosing and managing advanced periodontitis. Clinical laboratories use molecular techniques, such as Polymerase Chain Reaction (PCR) testing, to detect the bacterium’s genetic material in plaque samples collected from deep periodontal pockets. Another method relies on the bacterium’s unique enzymatic activity; T. forsythia exhibits trypsin-like activity, which can be rapidly detected using the chair-side BANA test.
Treatment protocols are designed to reduce the bacterial load and manage the resultant inflammation. The primary therapeutic approach is mechanical debridement, specifically scaling and root planing, which physically removes the subgingival plaque biofilm where the bacterium resides. This procedure aims to reduce the pocket depth and eliminate the anaerobic conditions that favor T. forsythia growth.
In cases of aggressive or persistent infection, mechanical treatment is often supplemented with targeted antibiotic therapy. Systemic antibiotics, such as a combination of amoxicillin and metronidazole, are commonly prescribed to reach the bacteria within the deep tissues. However, treating this infection can be complex, as some strains of T. forsythia possess genes, like tet(Q), that confer resistance to certain antibiotics, including tetracyclines.