From Biomechanics to Metallobiology: A Bibliometric Mapping of Ferroptosis and Trace Elements in Osteoarthritis (2014–2024)

Osteoarthritis (OA) is clinically characterized by progressive cartilage degradation and subchondral bone remodeling. However, the conventional “wear-and-tear” model fails to account for the metabolic drivers of this degeneration, resulting in a persistent therapeutic void. This study delineates a critical paradigm shift in orthopaedic scholarship: the transition from mechanical determinism to a molecular framework governed by Metallobiology and trace element homeostasis. We executed a systematic bibliometric analysis of 570 peer-reviewed articles indexed in Scopus (2014–2024), manually curated by clinical experts. By synthesizing keyword co-occurrence networks with patent landscape analysis, we visualized the intellectual evolution of ferroptosis, an iron-dependent form of regulated cell death, within the context of joint pathology. The data reveals an exponential growth in research output, predominantly driven by contributions from Mainland China (62%), reflecting a strategic pivot toward metabolic and botanical interventions. Keyword clustering identifies three thematic pillars: molecular redox mechanisms, metabolic animal models, and therapeutic chelation. These clusters collectively define the “Trace Element-Joint Axis,” establishing the joint not merely as a mechanical bearing but as a distinct metabolic repository susceptible to metal ion dysregulation. Specifically, the literature underscores how chondrocyte viability is increasingly associated with the host’s metallomic profile, contingent upon the delicate balance between systemic iron overload and selenium-dependent GPX4 activity. Furthermore, patent analysis indicates a translational surge toward “Metallobiological Interventions,” moving beyond structural repair to target upstream redox imbalances. We propose “Metallobiological Orthopaedics” as a clinical framework dedicated to restoring metallostasis and trace element homeostasis to potentially modulate cartilage degradation. This bibliometric analysis highlights a significant paradigm shift, indicating that osteoarthritis progression is heavily influenced by trace element dyshomeostasis alongside traditional factors like senescence. Consequently, future therapeutic strategies should expand beyond local biomechanical management to encompass the systemic regulation of the metallome. The ultimate goal is to treat osteoarthritis and mitigate oxidative toxicity by optimizing the patient’s iron-selenium equilibrium.