Periodontal dysbiosis in a healthy control subject later affected by subarachnoid hemorrhage: A case report.

Periodontal dysbiosis is characterized by a shift towards specific obligate anaerobic bacteria, capable of inducing persistent, low-grade systemic inflammation. Increasing evidence links oral anaerobes to increased vascular risk and neuroinflammatory pathways. We present the case of a 45-year-old, previously healthy, Caucasian male, enrolled as a control subject in a prospective clinical study, exhibiting poor oral hygiene, generalized gingival inflammation, bleeding on probing: 56.79%, plaque index: 85.18%, and a 7 mm periodontal pocket. Anaerobic culture from subgingival plaque sampling revealed the presence of Porphyromonas gingivalis, Fusobacterium nucleatum, Prevotella buccae, Veillonella parvula and Veillonella rogosae (V. rogosae). Concurrently, elevated serum high-sensitivity C-reactive protein (hsCRP) (6.3 mg L-1) was also detected. Prior to scheduled follow-up, the patient developed a spontaneous subarachnoid hemorrhage, where neuroimaging and angiography did not identify a vascular source. After recovery, periodontal therapy and cessation of all tobacco products, subgingival anaerobic diversity markedly decreased, with persistent detection of V. rogosae only; in addition, hsCRP also normalized. Although causality cannot be established, our case highlights systemic inflammatory implications of periodontal dysbiosis - and underlying neuroinflammatory processes - and demonstrates that periodontal therapy may be crucial in normalizing systemic inflammatory markers, effectively contributing a decreased disease burden through multiple pathways.