Biochemistry of periodontal diseases

Lídice Karla Santi-Garrido, Roxana Arjona-Leyva, Roxanet Ramírez-Ramírez and Yanelilian Padín-Gámez

SAP Dentistry, 2026

Abstract: Periodontal diseases are chronic inflammatory conditions of multifactorial origin, primarily caused by bacteria such as Porphyromonas gingivalis and exacerbated by risk factors such as poor oral hygiene, smoking, diabetes, obesity, and stress. Their historical evolution shows progress from ancient conceptions to the current scientific approach, highlighting the role of biochemistry in understanding their etiology. The objective of this literature review was to analyze the pathological mechanisms of periodontal diseases from a biochemical perspective to understand their etiology, diagnosis, and treatment. During the research process, the following methods were used: document analysis, systems approach, historical-logical analysis, analytical-synthetic analysis, and inductive-deductive reasoning. A total of 10 international, national, and regional bibliographies were reviewed. The immune response triggered by bacterial plaque generates inflammatory mediators (cytokines, prostaglandins) that cause tissue destruction and bone loss. Furthermore, there is a bidirectional relationship between periodontal disease and systemic diseases (cardiovascular disease, diabetes), reinforcing its relevance to public health. Treatments vary according to severity, ranging from scaling and root planing to regenerative surgery. Prevention, through proper oral hygiene, regular dental visits, and a healthy lifestyle, is key. Periodontal disease poses a significant public health challenge, and its study from a biochemical perspective offers crucial opportunities for addressing it. A holistic approach, integrating biology, biochemistry, and social care, will improve the diagnosis, treatment, and prevention of these diseases, benefiting both oral and general health.

Date: 2026
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Persistent link: https://EconPapers.repec.org/RePEc:cwf:dentar:dent2026173

DOI: 10.62486/dent2026173

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