Cadmium exposure leads to bone toxicity through its disruption of osteoclast and osteoblast functions. The study stresses the importance of regulating cadmium in the environment to protect bone health in both humans and animals.
Authors
- He, S., & Zhang, K. (2025). , Biology, 14(8), 1051.
What was issued?
The review focuses on the harmful effects of cadmium exposure on bone health, particularly how cadmium disrupts bone remodeling. The paper delves into the mechanisms of cadmium-induced bone damage by examining the critical balance between osteoclasts (OCs), which resorb bone, and osteoblasts (OBs), which form new bone. Cadmium exposure impairs osteoblast differentiation and promotes excessive osteoclast activation, resulting in diseases such as osteoporosis and osteomalacia. The review highlights the complex cellular interactions and signals, including the disruption of the RANKL/OPG axis, oxidative stress, and mitochondrial dysfunction, all contributing to bone toxicity.
Who is affected?
This research affects various populations, especially those exposed to cadmium through environmental contamination or industrial activities. Specifically, wildlife, livestock, and humans in areas with high cadmium pollution may suffer from bone health deterioration. Populations at greater risk include the elderly, smokers, and those with pre-existing bone conditions or poor nutritional status. It also applies to food safety professionals, environmental health experts, and animal health researchers, all of whom must consider cadmium exposure’s effects on bone health.
Most important findings
The most critical finding from this review is the detailed understanding of how cadmium affects osteoclast and osteoblast activity, leading to bone loss. Cadmium promotes osteoclast formation by altering the RANKL/OPG balance and increasing the production of pro-inflammatory cytokines. Additionally, cadmium directly impairs osteoblast differentiation, function, and survival, especially through mitochondrial damage and oxidative stress. The disruption of osteoclast-osteoblast communication, which is essential for bone remodeling, leads to increased bone resorption and decreased bone formation. The review also outlines interventions under study in animal models, such as antioxidants (for example N-acetylcysteine and melatonin) and anti-resorptive agents such as bisphosphonates, as research directions for counteracting cadmium’s effects on bone.
Key implications
The findings of this review clarify how cadmium, a persistent contaminant that bioaccumulates through the food chain, damages bone by disrupting the communication between bone-resorbing osteoclasts and bone-forming osteoblasts. The authors present this mechanistic understanding as a foundation for identifying therapeutic targets to mitigate cadmium bone toxicity in animals and for informing ecological risk assessment and management in contaminated environments. Because the evidence comes from animal models and cell studies, it does not by itself set limits for cadmium in food.
Citation
He, S., & Zhang, K. (2025). Cadmium-Induced Bone Toxicity: Deciphering the Osteoclast–Osteoblast Crosstalk. Biology, 14(8), 1051. https://doi.org/10.3390/biology14081051
Cadmium is a persistent heavy metal that accumulates in kidneys and bones. Dietary sources include cereals, cocoa, shellfish and vegetables, while smokers and industrial workers receive higher exposures. Studies link cadmium to kidney dysfunction, bone fractures and cancer.