ONNA-SON, Japan: The ability of Porphyromonas gingivalis to colonise the oral cavity depends partly on a short surface filament that helps it attach to other bacteria, become established in biofilms and limit recognition by the host immune system. A new study has examined how the filament forms and supports these processes. The researchers identified several vulnerable features of the filament that could provide targets for future periodontal therapies.
The filament, known as the Mfa pilus, has a main shaft assembled from multiple copies of a protein called Mfa1. The researchers found that even very small alterations to one end of Mfa1 prevented the filament from forming. Interfering with this process could therefore limit the ability of P. gingivalis to colonise the oral cavity.
A separate region of the filament appeared to reduce recognition of P. gingivalis by the host immune system. When the researchers altered the region’s ability to bind to calcium, cultured human cells produced a stronger inflammatory response. This suggests that calcium binding may help P. gingivalis evade innate immune responses.
Another significant finding concerns the interaction of P. gingivalis with other bacteria in oral biofilms. The study identified the location and structure of a region of Mfa1 that previous research had implicated in binding to a surface protein of Streptococcus gordonii, an early coloniser of tooth surfaces. Because this interaction is known to promote mixed-species biofilm development, the finding could support the development of molecules capable of disrupting bacterial adhesion and preventing biofilm maturation.
These findings provide valuable mechanistic insight into one of the key virulence factors of P. gingivalis. By showing how the Mfa pilus forms, affects immune recognition and helps P. gingivalis attach to other bacteria, the study identifies several potential therapeutic targets. This potential is supported by recent research demonstrating that antibodies directed against Mfa1 can reduce bacterial levels and alveolar bone loss in rats, highlighting Mfa1 as a promising therapeutic target.
Strategies that prevent the Mfa pilus from forming, interfere with its ability to alter immune recognition or block the attachment of P. gingivalis to other bacteria could offer new ways to prevent periodontal biofilm formation and disease progression. Given the growing evidence linking P. gingivalis with systemic conditions, including cardiovascular disease, diabetes and Alzheimer’s disease, therapies developed from the study findings could have benefits extending beyond oral health.
The paper, titled “Cryo-EM structure of the native assembled Mfa Type V pilus from the periodontal pathogen Porphyromonas gingivalis”, was published online on 24 June 2026 in Communications Biology, ahead of inclusion in an issue.
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