26dkou366 10.3205/26dkou366 urn:nbn:de:0183-26dkou3662 Meeting Abstract Hofbeck Hofbeck Luca L

Department of Orthopaedics and Trauma Surgery, University Hospital Erlangen, Erlangen, Deutschland

author Haller Haller Daniel D

Neuromuscular Physiology and Neural Interfacing Laboratory, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Deutschland

author Betsch Betsch Marcel M

Department of Orthopaedics and Trauma Surgery, University Hospital Erlangen, Erlangen, Deutschland

author Boosz Boosz Philipp P

Department of Orthopaedics and Trauma Surgery, University Hospital Erlangen, Erlangen, Deutschland

author Del Vecchio Del Vecchio Alessandro A

Neuromuscular Physiology and Neural Interfacing Laboratory, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, 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 366 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 | Tribologie & Gelenke Berlin 20261020 20261023 DKOU26_Abs_2417 TextObjectives and questions: Quadriceps dysfunction is hallmark of end-stage knee osteoarthritis (KOA) and contributes substantially to functional limitations and reduced quality of life. While mechanical joint degeneration and disuse are well-recognized contributors, growing evidence indicates that neural alterations may also play a critical role in observed force deficits. However, the organization of motor unit discharge behavior and the extent of common synaptic input in individuals with advanced KOA remain insufficiently characterized. A deeper understanding of these neural control mechanisms is clinically relevant, as they may explain the characteristic quadriceps weakness and impaired motor performance in KOA. Furthermore, identifying disease-specific alterations in neural drive could inform the development of targeted pre- and postoperative rehabilitation strategies aimed at restoring muscle function more effectively.Material and methods: In this hypothesis-driven, controlled cross-sectional case–control pilot study, intramuscular electromyography was recorded from the vastus medialis (VM) and vastus lateralis (VL) during repeated (5×30 s) isometric knee extensions performed at 10% and 20% of maximal voluntary contraction (MVC). The KOA group comprised 10 patients with end-stage KOA (Kellgren–Lawrence 4) (mean age 66±6 years; 7 female, 3 male). The control group included 10 age-matched individuals without prior history of knee pathology (mean age 64±5 years; 6 female, 4 male). Motor unit spike trains were decomposed offline and concatenated across steady-force plateaus for each participant. Intramuscular coherence was calculated from cumulative spike trains (CST) using CST splitting. Coherence with the δ-band (1–5 Hz) was defined a priori as the the primary outcome measure. Between-group differences were analyzed using Mann–Whitney U tests,and rank-biserial correlations were reported as effect sizes (α = 0.05).Results: For the VL, δ-band coherence (1–5 Hz) did not differ between groups (median 0.203 in OA vs. 0.172 in controls; p = 1.00). In contrast, VM δ-band coherence at 10% MVC tended to be lower in the OA group (median 0.154 vs. 0.272), corresponding to a moderate rank-biserial effect size (rB = 0.50), although this difference did not reach statistical significance (p = 0.34). Similarly, the intermuscular VM–VL coherence difference was not significantly different between groups (p = 0.49).Discussion and conclusions: The results of this study indicate a muscle-specific alteration in neural drive in end-stage KOA, characterized by reduced low-frequency common synaptic input to the vastus medialis. The observed effect size suggests a clinically meaningful neurophysiological difference, supporting the concept that quadriceps weakness in advanced KOA reflects altered central motor control rather than purely structural joint degeneration. These results highlight neural control mechanisms as a potential therapeutic target for optimizing neuromuscular rehabilitation in patients undergoing total knee arthroplasty. 0 0 0 0