Further studies, including anti-CCP and anti-ENO1 antibodies, in addition to other types of ACPAs such as anti-fibrinogen, anti-vimentin, or anti-CEP-1 antibodies could help to clarify the role of periodontitis and periodontal pathogens, such as P. gingivalis and A. actinomycetemcomitans in ACPA formation in RA patients, as well as their relationship with rheumatoid clinical variables. This evidence concerns the gene VIM and rheumatoid arthritis.