Mechanoinflammation in osteoarthritis: knowledge evolution, cellular interactions, and translational research priorities.

Abstract

Background: Osteoarthritis (OA) is increasingly recognized as a whole-joint disorder in which mechanical stress, cellular mechanosensing, and inflammatory responses interact across joint tissues. Although OA mechanoinflammation has attracted growing attention, its literature remains distributed across mechanobiology, inflammation research, molecular medicine, and translational research. This study aimed to map the knowledge structure and temporal development of OA mechanoinflammation and to characterize relationships among mechanosensing, inflammatory responses, tissue crosstalk, and emerging research priorities.

Methods: Publications related to OA mechanoinflammation were retrieved from the Web of Science Core Collection and PubMed from January 1, 2000 to May 23, 2026. Bibliometric and knowledge-map analyses characterized publication trends, collaboration patterns, reference co-citation structures, author keyword themes, journal-level knowledge flows, and sensitivity to database source, retrieval dependence, and clustering parameters. Keyword-reference correspondence was evaluated using year-stratified permutation testing and bootstrap confidence intervals, and temporal use of reference clusters was assessed using an annual citation-opportunity-adjusted analysis.

Results: Research output increased markedly in recent years. Under the primary analytical configuration, reference co-citation and author keyword analyses each yielded four interpretable intermediate-resolution domains. Validated keyword-reference correspondence identified selective relationships linking mechanotransduction-related themes with the mechanical-loading and mechanosensitive-channel knowledge bases, together with a significant relationship between the broader inflammatory-degeneration theme and contemporary OA pathogenesis, aging, and tissue crosstalk. After adjustment for citation opportunity, recent years showed greater relative use of the contemporary OA/tissue-crosstalk and mechanosensitive-channel reference domains, with substantial year-to-year heterogeneity. Sensitivity analyses showed high stability of the principal reference-based structures and identified greater variability at keyword-domain boundaries.

Conclusions: OA mechanoinflammation is an expanding interdisciplinary research area linking mechanical context, cellular mechanosensing, inflammatory responses, and whole-joint remodeling at the literature level. The mapped structures and recent temporal patterns identify testable priorities for multimodal phenotyping, biomarker validation, mechanistically relevant models, and combined mechanical-inflammatory intervention research. These translational directions remain hypothesis-generating and require prospective experimental and clinical validation.