Abstract: SA-PO0546
Effect of CKD on Periodontal Remodelling: Mechanisms and Clinical Relevance
Session Information
- CKD: Clinical - Therapies, CKM Health, Special Populations, and More
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2202 CKD (Non-Dialysis): Clinical, Outcomes, and Trials
Authors
- Wolf, Michael, Rheinisch-Westfalische Technische Hochschule Aachen, Aachen, NRW, Germany
- Wu, Zhuojun, Rheinisch-Westfalische Technische Hochschule Aachen, Aachen, NRW, Germany
- Jankowski, Vera, Rheinisch-Westfalische Technische Hochschule Aachen, Aachen, NRW, Germany
- Jankowski, Joachim, Rheinisch-Westfalische Technische Hochschule Aachen, Aachen, NRW, Germany
Group or Team Name
- UKAachen
Background
Periodontal remodelling is a continuous and tightly regulated process required to maintain the structural and functional integrity of periodontal tissues. Although local factors such as bacterial biofilm accumulation, mechanical overload, and inadequate oral hygiene are established triggers of periodontal disease, they do not fully account for its high and persistent prevalence. Increasing evidence suggests that periodontal homeostasis is strongly influenced by systemic health status.
Methods
We highlight chronic kidney disease (CKD) as a major systemic driver of periodontal dysregulation and reframe periodontal disease as a manifestation of systemic inflammatory and metabolic dysfunction rather than a purely local bacterial condition. This presentation is conceptual in nature and structured as a narrative review. It synthesises current knowledge on molecular and cellular pathways linking CKD-associated systemic alterations to impaired periodontal remodelling and tissue homeostasis.
Results
Chronic kidney disease disrupts periodontal integrity through chronic inflammation, uraemic toxins, oxidative stress, and immune dysregulation, impairing fibroblast function, matrix turnover, vascularity, and osteogenesis. Disturbed calcium–phosphate balance and endothelial dysfunction further weaken mineralisation and regeneration. Similar mechanisms occur in cardiovascular, liver, hematologic, and diabetic diseases, collectively promoting a systemic state that drives periodontal impairment as a consequence of systemic dysfunction.
Conclusion
Recognition of CKD as a key systemic modulator of periodontal remodelling has important clinical implications, requiring intensified dental surveillance and interdisciplinary nephrology–periodontology care. Future research should identify early biomarkers and develop targeted interventions addressing shared inflammatory and metabolic pathways to reduce periodontal disease burden in affected patients.