26dkou404 10.3205/26dkou404 urn:nbn:de:0183-26dkou4049 Meeting Abstract Heller Heller Raban R

German Armed Forces Hospital Ulm, Department for Trauma Surgery and Orthopaedics, Reconstructive and Septic Surgery, Sportstraumatology, Ulm, Deutschland Technische Universität Berlin, Department of Food Chemistry and Toxicology, Berlin, Deutschland University Hospital of Ulm, Institute of Clinical and Experimental Trauma–Immunology, Ulm, Deutschland

author Maares Maares Maria M

Institute of Nutritional Science, Department of Food Chemistry, Potsdam, Deutschland Technische Universität Berlin, Department of Food Chemistry and Toxicology, Berlin, Deutschland

author Alhalabi Alhalabi Obada T. OT

Heidelberg University Hospital, Department of Neurosurgery, Heidelberg, Deutschland Heidelberg University, Medical Faculty, Heidelberg, Deutschland

author Mannes Mannes Marco M

University Hospital of Ulm, Institute of Clinical and Experimental Trauma-Immunology, Ulm, Deutschland

author Krieg Krieg Sandro M. SM

Heidelberg University Hospital, Department of Neurosurgery, Heidelberg, Deutschland Heidelberg University, Medical Faculty, Heidelberg, Deutschland

author Achatz Achatz Gerhard G

German Armed Forces Hospital Ulm, Department for Trauma Surgery and Orthopaedics, Reconstructive and Septic Surgery, Sportstraumatology, Ulm, Deutschland

author Haase Haase Hajo H

Technische Universität Berlin, Department of Food Chemistry and Toxicology, Berlin, Deutschland

author Schomburg Schomburg Lutz L

Charité – Universitätsmedizin Berlin, Institute for Experimental Endocrinology, Berlin, Deutschland

author Moghaddam Moghaddam Arash A

Orthopedic and Trauma Surgery, Aschaffenburg, Deutschland

author Biglari Biglari Bahram B

BG Trauma Centre Ludwigshafen, Department of Paraplegiology, Ludwigshafen, Deutschland

author Younsi Younsi Alexander A

Heidelberg University Hospital, Department of Neurosurgery, Heidelberg, Deutschland Heidelberg University, Medical Faculty, Heidelberg, Deutschland BG Trauma Centre Ludwigshafen, Department of Neurosurgery, Ludwigshafen, Deutschland

author German Medical Science GMS Publishing House

Düsseldorf

610 20261020 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0659 404 Deutsche Gesellschaft für Orthopädie und Unfallchirurgie Deutsche Gesellschaft für Orthopädie und Orthopädische Chirurgie Deutsche Gesellschaft für Unfallchirurgie Berufsverband für Orthopädie und Unfallchirurgie Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2026) Grundlagenforschung | Trauma und Inflammation 1 Berlin 20261020 20261023 DKOU26_Abs_2455 TextObjectives and questions: Zinc homeostasis is closely associated with neuroinflammation and oxidative stress after traumatic spinal cord injury (TSCI). While clinical studies suggest the diagnostic relevance of zinc dynamics, translational animal data connecting total zinc (Zn) and free zinc (fZn) to neurological recovery are limited. We aimed to characterize early serum Zn and fZn trajectories in a controlled rodent TSCI model and evaluate their predictive values for neurological outcomes.Material and methods: Longitudinal assessment of a rat thoracic compression–contusion spinal cord injury model (n=120; 80 SCI, 40 controls; all female) was conducted at 1, 3, 7, 14, and 28 days post-injury (dpi). Serum Zn, fZn, and selenium were quantified and related to functional recovery using BBB score stratification. Group differences were assessed nonparametrically. Univariate logistic regression with receiver operating characteristic (ROC) analysis was used to evaluate the predictive performance of spinal cord impairment.Results: TSCI induces an immediate disruption of zinc homeostasis. At 1 dpi, animals with poor neurological recovery showed significantly lower Zn and fZn levels than recovering animals and shams. fZn demonstrated the strongest early stage group separation. Depressed zinc metrics persisted in animals without recovery. Predictive modeling revealed a high early diagnostic accuracy. At 1 dpi, fZn achieved an AUC of 0.94 (95\'25 CI 0.82–1.00), outperforming total Zn (AUC 0.85, 0.67–1.00). At 3 dpi, fZn remained predictive (AUC 0.88, 0.72–1.00). The strongest performance occurred at 7 dpi, where fZn reached an AUC of 0.96 (0.89–1.00), indicating near-perfect discrimination of neurological impairments. Animals with higher early fZn levels demonstrated accelerated functional gain (p < 0.01 at 7 dpi; p < 0.05 at 28 dpi). Correlation analyses showed stable coupling between total Zn and fZn over time, but fZn tracked additional information on functional recovery. The Zn/fZn ratio did not provide any additional discriminatory value.Discussion and conclusions: Early disruption of zinc homeostasis represents a translational biomarker signature of neurological outcomes after TSCI and highlights a central interface with trauma immunology. Free zinc is a sensitive early indicator of excellent predictive performance and a strong association with functional recovery. The rodent model complements human observations and identifies a critical early window in which zinc dynamics may guide prognostic stratification and future therapeutic targets. 0 0 0 0