Summary
It is abundantly obvious that the uncontrolled degradation and/or activation of host defense pathways is the major pathway by which the periodontal pathogen P. gingivalis promotes its growth and proliferation. By being able to shed host receptors, degrade cytokines, and activate coagulation, complement, and kallikrein/kinin pathways it is clear that this organism has found a mechanism(s) to evade host defense and at the same time develop a system for cannibalizing host proteins for its own nutritional usage (Fig 2). Thus, it seems only logical that the development of inhibitors against these bacterial proteinases would be a useful method for negating their activities and making such pathogens more susceptible to attack by host phagocyte cells. In this respect, the structure of the truncated form of RGP has just been elucidated. Thus, it should only be a question of time before inhibitors to this enzyme will be developed and, hopefully, be used to reduce the pathologies associated with the development of periodontitis and/or eliminate the disease altogether.
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Travis, J., Banbula, A., Potempa, J. (2002). The Role of Bacterial and Host Proteinases in Periodontal Disease. In: Langner, J., Ansorge, S. (eds) Cellular Peptidases in Immune Functions and Diseases 2. Advances in Experimental Medicine and Biology, vol 477. Springer, Boston, MA. https://doi.org/10.1007/0-306-46826-3_46
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DOI: https://doi.org/10.1007/0-306-46826-3_46
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