Autophagy as a potential mechanism underlying the biological effect of 1,25-Dihydroxyvitamin D3 on periodontitis: a narrative review

Abstract

The major active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25D3), is known for its wide bioactivity in periodontal tissues. Although the exact mechanisms underlying its protective action against periodontitis remain unclear, recent studies have shown that 1,25D3 regulates autophagy. Autophagy is vital for intracellular pathogen invasion control, inflammation regulation, and bone metabolic balance in periodontal tissue homeostasis, and its regulation could be an interesting pathway for future periodontal studies. Since vitamin D deficiency is a worldwide health problem, its role as a potential regulator of autophagy provides new insights into periodontal diseases. Based on this premise, this narrative literature review aimed to investigate the possible connection between 1,25D3 and autophagy in periodontitis. A comprehensive literature search was conducted on PubMed using the following keywords (e.g., vitamin D, autophagy, periodontitis, pathogens, epithelial cells, immunity, inflammation, and bone loss). In this review, the latest studies on the protective action of 1,25D3 against periodontitis and the regulation of autophagy by 1,25D3 are summarized, and the potential role of 1,25D3-activated autophagy in the pathogenesis of periodontitis is analyzed. 1,25D3 can exert a protective effect against periodontitis through different signaling pathways in the pathogenesis of periodontitis, and at least part of this regulatory effect is achieved through the activation of the autophagic response. This review will help clarify the relationship between 1,25D3 and autophagy in the homeostasis of periodontal tissues and provide perspectives for researchers to optimize prevention and treatment strategies in the future.

METTL3 Promotes Osteogenic Differentiation of Human Periodontal Ligament Stem Cells through IGF2BP1-Mediated Regulation of Runx2 Stability

“…The treatment of periodontitis aims at promoting the regeneration of alveolar bone tissue as much as possible after plaque removal [22]. Osteogenic differentiation of hPDLSCs is an important process of alveolar bone formation [23].…”

A case of early-onset periodontitis with vitamin D deficiency: A case report and literature review

“…Evidence suggests that vitamin D is anti-inflammatory through inhibition of the NF-κB/NLRP3 signaling pathway. [34] Subsequent IL-1β and reactive oxygen species decrease to hinder the progression of periodontitis. [34] The deficiency of vitamin D would contribute to the CD4 + / CD8 + reduction, which could reflect cellular immune dysfunction.…”

“…[34] Subsequent IL-1β and reactive oxygen species decrease to hinder the progression of periodontitis. [34] The deficiency of vitamin D would contribute to the CD4 + / CD8 + reduction, which could reflect cellular immune dysfunction. The ratio of CD4 + (helper or regulatory CD4 + T cells)/CD8 + (cytotoxic CD8 + T cells) is an important indicator, reflecting the activity of T lymphocytes as well as the body's overall immune function and disease development.…”

“…Evidence suggests that vitamin D is anti-inflammatory through inhibition of the NF-κB/NLRP3 signaling pathway. [ 34 ] Subsequent IL-1β and reactive oxygen species decrease to hinder the progression of periodontitis. [ 34 ]…”

“…[ 34 ] Subsequent IL-1β and reactive oxygen species decrease to hinder the progression of periodontitis. [ 34 ]…”