OSF Preprints
Medial meniscal extrusion in knee osteoarthritis: prognostic marker, biomechanical mediator, or modifiable target? A systematic review and evidence map
Par Yong Huang et 万力畅.
Contenu en anglais
Résumé
Medial meniscal extrusion (MME) is common in knee osteoarthritis (OA), yet its causal role remains unresolved: it may precede and contribute to abnormal tibiofemoral load transfer, serve primarily as an imaging marker of pre-existing meniscal, cartilage, bone or alignment pathology, arise as a consequence of established structural disease, or represent a modifiable treatment target. Recent randomized and meta-analytic evidence on meniscal centralization after posterior root repair has intensified rather than settled this debate. This systematic review and evidence map will examine symptomatic, non-end-stage knee OA (Kellgren–Lawrence grades 0–3, with KL 0–1 requiring symptoms plus MRI-defined early structural abnormality or a validated early-OA classification). Three questions are addressed: (RQ1) how MME is defined, measured and associated with structural and symptomatic progression; (RQ2) which experimental studies support MME as an intermediate phenotype of abnormal load transfer; (RQ3) whether interventions that alter MME also improve mechanical endpoints, structural outcomes and patient-reported outcomes. Seven databases (PubMed/MEDLINE, Embase, Web of Science, Scopus, Cochrane CENTRAL, CNKI, Wanfang) and three trial registries will be searched without language restriction. Evidence will be mapped across five domains ordered by causal proximity, from direct cadaveric and finite-element manipulation studies to clinical intervention trials. Meta-analysis will be restricted to studies comparable in imaging platform, loading state, MME definition and follow-up window; certainty will be graded with GRADE for human outcomes and a prespecified mechanistic certainty matrix for experimental evidence. Reverse causality, indication confounding, measurement-state heterogeneity and bilateral-knee dependence are addressed through a time-indexed causal DAG and prespecified sensitivity analyses.



