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Treponema denticola is a Gram-negative, obligate anaerobic, motile spirochete that is a primary etiological agent in the development of severe periodontal disease [1, 2]. It is a member of the "red complex," a group of bacteria categorized by their high virulence and strong association with chronic periodontitis [3, 6]. The organism possesses several virulence factors, including the major surface protein (Msp) for adhesion and dentilisin, a chymotrypsin-like protease that degrades host proteins and modulates immune responses [2, 3]. While not a single molecular target, T. denticola is the focus of antimicrobial strategies aimed at treating oral infections [5]. Recent research has also implicated its presence in systemic conditions such as cardiovascular disease and Alzheimer's disease due to its ability to enter the bloodstream and cross the blood-brain barrier [4]. Therapeutic intervention typically involves mechanical debridement combined with systemic or local antibiotics to reduce the bacterial load [5]. Understanding its metabolic pathways and surface proteins remains crucial for developing targeted narrow-spectrum therapies [1].
Inhibition of DNA synthesis (Metronidazole), inhibition of bacterial cell wall synthesis (Amoxicillin), inhibition of protein synthesis via the 30S ribosomal subunit (Tetracyclines), and non-specific disruption of bacterial membranes (Chlorhexidine) [5, 6].
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