Vitamin D2026-05

Vitamin D Deficiency as a Context-Dependent Modifier of Osteonecrosis of the Jaw.

Lu Chien-Lin, Huang Ren-Yeong, Zheng Cai-Mei, Lu Kuo-Cheng — Nutrients

Summary

This review suggests that not having enough vitamin D might make some people more vulnerable to a serious jaw bone condition called osteonecrosis of the jaw (ONJ). It acts as a contributing factor, especially when other health issues are present, rather than being the sole cause. Maintaining adequate vitamin D levels could potentially support jaw health.

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Key points

Vitamin D deficiency may increase vulnerability to osteonecrosis of the jaw (ONJ).
It acts as a contributing factor, not a primary cause, especially when other risk factors are present.
Vitamin D affects bone healing, inflammation, and blood vessel health in the jaw.
More research is needed to confirm these findings in human studies.

What the study looked at

This review explored how vitamin D might be involved in osteonecrosis of the jaw (ONJ), a complex condition where jaw bone tissue dies. Researchers wanted to understand if and how vitamin D deficiency contributes to this problem. This was a comprehensive review that gathered and analyzed existing scientific information from various sources. It looked at studies on how vitamin D works at a cellular level, animal experiments, and observational studies involving people. It did not involve new experiments or participants. What it found: The review proposes that low vitamin D levels don't directly cause ONJ but can make someone more susceptible to it, especially when other health issues or treatments are present. Vitamin D deficiency might impair bone repair, increase inflammation, and affect blood vessel health in the jaw, creating an environment where ONJ is more likely to develop or worsen.

Dietary takeaway

While this review highlights a potential link, it's important to remember that it synthesizes existing research and isn't a definitive new study. Ensuring adequate vitamin D intake through diet (like fatty fish, fortified foods) and safe sun exposure is generally beneficial for overall bone health. However, more direct research is needed to confirm if specific vitamin D levels or supplementation can prevent or treat ONJ.

Abstract

Osteonecrosis of the jaw (ONJ) is a multifactorial disorder characterized by impaired bone remodeling, vascular compromise, immune dysregulation, and mucosal barrier disruption. Although these mechanisms have been extensively investigated, they are often discussed separately, limiting an integrated understanding of ONJ pathogenesis. Vitamin D has emerged as a biologically relevant factor across these interconnected pathways, yet its role in ONJ remains incompletely defined. This narrative and hypothesis-generating review synthesizes current mechanistic, preclinical, observational, and clinical evidence regarding vitamin D biology and ONJ and proposes a vitamin D-centered vulnerability model in which vitamin D deficiency acts as a context-dependent modifier rather than a primary causal driver. Mechanistically, vitamin D deficiency may impair osteoblast function and mineralization, disrupt angiogenic responses, promote pro-inflammatory immune signaling, and compromise mucosal integrity, collectively creating a microenvironment susceptible to impaired healing and osteonecrosis. These effects are likely to vary across clinical settings, particularly in patients receiving antiresorptive or antiangiogenic therapies. Clinical and epidemiological studies have reported associations between low vitamin D status and increased ONJ risk or severity, while some observational studies suggest that vitamin D supplementation may be associated with improved outcomes in selected populations. However, current human evidence remains predominantly observational and subject to substantial heterogeneity and residual confounding, and direct randomized evidence is lacking. Overall, this framework provides an integrated perspective linking vitamin D biology to ONJ-related pathogenic processes and may support future mechanistic research, risk stratification, and supportive multidisciplinary management strategies. Nevertheless, the proposed model should be interpreted cautiously as hypothesis-generating and requires further validation in well-designed prospective studies and randomized controlled trials.

View on PubMed →DOI: 10.3390/nu18111769