Yakymchuk M. M., Pynda M. Ya., Yakymchuk O. M.
REDOX-IMMUNE MECHANISMS OF ALVEOLAR BONE REMODELING IN GENERALIZED PERIODONTITIS UNDER THYROID DYSFUNCTION: CURRENT PATHOGENETIC PERSPECTIVES
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About the author:
Yakymchuk M. M., Pynda M. Ya., Yakymchuk O. M.
Heading:
LITERATURE REVIEWS
Type of article:
Scientific article
Annotation:
Generalized periodontitis is a chronic immune-inflammatory disease in which the microbial challenge initiates but does not fully determine the extent of tissue destruction. Host-response characteristics, systemic metabolic background, and regenerative capacity substantially influence disease progression. The aim of this review was to summarize current evidence on oxidative stress, cytokine dysregulation, and osteoimmune mechanisms in periodontitis and to assess how thyroid dysfunction may modify these pathways. A structured narrative analysis of peer-reviewed publications from 2020 to 2026 was performed, focusing on periodontal pathogenesis, thyroid regulation of bone, reactive oxygen species, the RANK/RANKL/OPG system, inflammatory cytokines, and clinical associations between thyroid diseases and periodontal status. Excessive generation of reactive oxygen species during periodontal inflammation can activate NF-kB, MAPK, and other redox-sensitive signaling pathways, sustain the production of IL-1β, IL-6, and TNF-α, enhance extracellular-matrix proteolysis, and promote RANKL-dependent osteoclastogenesis. Thyroid hormones and thyrotropin additionally regulate bone turnover, cellular energy metabolism, and osteogenic differentiation of periodontal ligament cells. Experimental models demonstrate that periodontitis combined with hyperthyroidism is accompanied by a more pronounced increase in TNF-α and IL-1β, whereas both hypo- and hyperthyroid states aggravate biochemical signs of connective-tissue degradation. Systematic reviews and meta-analyses published in 2024-2025 generally report worse probing depth and clinical attachment loss in patients with thyroid disease, although heterogeneity of the primary studies precludes interpretation of this association as proven unidirectional causality. The most plausible model is that thyroid dysfunction modifies the metabolic and redox environment in which periodontal inflammation develops, thereby changing the magnitude of osteoimmune responses and the regenerative potential of periodontal tissues. Future experimental work should simultaneously evaluate oxidative-stress and antioxidant markers, TNF-α, IL-1β, IL-6, IL-10, RANKL/OPG, bone-turnover markers, and morphological periodontal changes in clearly separated models of hypothyroidism and hyperthyroidism.
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Publication of the article:
«Bulletin of problems biology and medicine», 2026 Issue 3, 182, 161-167 pages, index UDC 616.314.17-008.1-092:616.441-008.6:612.015.1