Periodontal Dysbiosis and Psoriatic Arthritis: From Oral Threshold Modification to Post-Enthesitic Synovial Amplification

Abstract

Abstract Background Psoriatic arthritis (PsA) is not well explained by directly importing the Porphyromonas gingivalis–PPAD–ACPA model from rheumatoid arthritis (RA): PsA is usually seronegative and has an enthesis-centered anatomy. This note develops a distinct hypothesis: chronic periodontal dysbiosis may generate repeated systemic microbial and innate-immune pulses that lower the inflammatory threshold at mechanically stressed entheses in predisposed people with psoriasis. A small 2024 saliva-sequencing study identified increased Aggregatibacter in PsA, offering a preliminary candidate rather than proof of a causal species. Scope The established PsA IL-23/IL-17/TNF axis, the clinical significance of enthesitis, and the association between periodontitis and psoriatic disease form the evidentiary base. The proposed two-hit oral-to-entesis pathway—periodontal dysbiosis → systemic innate priming (first hit) → mechanically stressed enthesis with DAMP release (second hit) → enthesitis—is explicitly hypothetical, as is a further proposed post-enthesitic stage in which an already-inflamed synovium may retain circulating oral bacterial material and amplify, without initiating, synovitis. It does not posit persistent bacterial infection of the joint.