Our current understanding of Fn pathogenesis is primarily derived from laboratory investigations using Fnn/Fnp strains.16–18,104–111 Due to extensive coaggregations with many other inflammophilic pathobionts,90,92–95Fn has been proposed to play a central role in promoting the formation of dysbiotic oral biofilms.112 For example, early work revealed that Fn abundance increases significantly during the onset of gingivitis,52 which is an inflammatory condition that precedes the chronic inflammation characterizing periodontitis. Here, FN1 is linked to periodontitis.