ArticleOrthopaedic surgery2026
Denosumab Regulates Titanium Particles-Induced Macrophages Inflammation and Osteolysis by Targeting the ST18/PARP1 Interaction.
Article in Orthopaedic surgery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Denosumab Regulates Titanium Particles-Induced Macrophages Inflammation and Osteolysis by Targeting the ST18/PARP1 Interaction.Orthopaedic surgery · 2026Article
- Case Report: Reconstruction of the chest wall with titanium alloy plates after resection of a rare malignant spindle cell tumor of the sternum complicated by ankylosing spondylitis.Frontiers in surgery · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
objectiveThis study aims to investigate the role of Denosumab and its downstream target ST18 in wear particle-induced macrophage inflammation and osteolysis, and to explore the underlying mechanisms involved in aseptic loosening (AL) of prosthetic joints.
methodsMacrophages were stimulated with titanium particles (TiPs), and inflammatory responses were assessed using qRT-PCR, western blot, flow cytometry, and immunohistochemistry. Denosumab's effects on inflammation and osteolysis were evaluated with the same approaches. Potential targets of Denosumab were screened via online databases and validated by qRT-PCR and western blot. ST18 was modulated in macrophages using lentiviral overexpression and knockdown systems. A mouse calvarial model of TiPs-induced osteolysis was established, and the roles of Denosumab and ST18 were examined in vivo using micro-CT, H&E staining, and tartrate-resistant acid phosphatase (TRACP) staining.
resultsDenosumab suppressed TiPs-induced macrophage inflammation by inhibiting NF-κB signaling and M1 polarization. We identified ST18 as a direct target of Denosumab, whose expression was upregulated by TiPs but downregulated by Denosumab. Lentivirus-mediated ST18 knockdown markedly attenuated TiPs-induced inflammation, whereas ST18 overexpression exacerbated it. Further analysis revealed that ST18 interacts with PARP1. In vivo, Denosumab significantly alleviated TiPs-induced osteolysis in mouse calvaria, an effect that was reversed by ST18 overexpression.
conclusionDenosumab attenuates TiPs-induced macrophage activation and osteolysis through suppression of the NF-κB pathway and M1 polarization, with ST18 serving as a key mediator. These findings highlight Denosumab as a promising therapeutic candidate for the prevention of prosthesis-related aseptic loosening.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.