A. A Treponema denticola cell observed by darkfield microscopy. Treponema denticola is a spirochete responsible for periodontitis. Bar: 5 µm.
B. A Treponema denticola cell undergoing cell division. The cell elongates and the two daughter cells sever. Bar: 5 µm.
C. Electron micrograph of the cell end after outer membrane removal by detergent treatment (sodium deoxycholate 1% for 10 minutes). After treatment the periplasmic flagellar filaments (PFF) are freed, and the cytoplasmic filaments (CF) can be observed. Bar: 1 µm (3).
Treponema are spirochetes, one of the few major bacterial groups whose natural phylogenic relationships are evident by gross phenotypic characteristics such as the morphology. The treponemes are responsible for a variety of diseases and are invasive due to their unique motility in dense media and their ability to penetrate cell monolayers. This feature is associated with their helical or wave-shaped cell body and the periplasmic flagellar filament location. Treponemes have in common a filamentous ribbon composed of two to six cytoplasmic filaments (3), which are involved in the cell division process (4).
As the gateway to the body, the mouth is challenged by a constant barrage of invaders: bacteria, viruses, parasites, and fungi. Infectious diseases, notably dental caries and periodontal diseases, predominate among the ills that can compromise oral health. The quantitative relationship between the presence of treponemes and the severity of periodontal disease has been shown (1, 5). Treponema denticola is one of the major spirochete species associated with the periodontitis pandemic (6). However, the treponemes involved are diverse in each unique patient mouth and among a population (2).
Darkfield microscopy is a contrast-enhancement technique to detect very small features by the light scatter of the observed object. It is required to observe treponemal cells due to the small diameter of the bacteria. The magnification required to observe periplasmic flagella and cytoplasmic filaments is provided by transmission electron microscopy.
References
1. Armitage, G. C., W. R. Dickinson, R. S. Jenderseck, S. M. Levine, and D. W. Chambers. 1982. Relationship between the percentage of subgingival spirochetes and the severity of periodontal disease. J. Periodontol. 53:550–556.
2. Choi, B. K., C. Wyss, and U. B. Gobel. 1996. Phylogenetic analysis of pathogen-related oral spirochetes. J. Clin. Microbiol. 34:1922–1925.
3. Izard, J., W. A. Samsonoff, M. B. Kinoshita, and R. J. Limberger. 1999. Genetic and structural analysis of the cytoplasmic filaments of wild-type and flagellar filament mutant of Treponema phagedenis. J. Bacteriol. 181:6739–6746.
4. Izard, J., W. A. Samsonoff, and R. J. Limberger. 2001. Cytoplasmic filament-deficient mutant of Treponema denticola has pleiotropic defects. J. Bacteriol. 183:1078–1084.
5. Moter, A., C. Hoenig, B. K. Choi, B. Riep, and U. B. Gobel. 1998. Molecular epidemiology of oral treponemes associated with periodontal disease. J. Clin. Microbiol. 36:1399–1403.
6. Simonson, L. G., C. H. Goodman, J. J. Bial, and H. E. Morton. 1988. Quantitative relationship of Treponema denticola to severity of periodontal disease. Infect. Immun. 56:726–728.
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