Preservation of Auxetic Oscillatory Capacity in Living Connective Tissue: An ECM-Regulated Hypothesis of Mechanical Homeostasis

Abstract

Living connective tissue preserves function while adapting to changing loads. This hypothesis proposes that preserving access to reversible auxetic deformation can contribute to mechanical homeostasis in selected tissues. Auxetic oscillation (AO) denotes repeated, reversible expression of negative-Poisson behavior; it does not require transitions between Poisson regimes. AO range is defined as the longitudinal-strain interval over which a directional incremental Poisson measure is reliably negative, with loading, unloading, recovery, and cycle stability described separately. The proposed biological contribution is that broader recoverable AO exposure produces cell–matrix inputs that better preserve extracellular-matrix (ECM) adaptability than an appropriately varied non-auxetic comparison. A bounded annulus-fibrosus example predicts less persistent matrix compaction after repeated AO exposure and defined recovery, as a candidate structural indicator of preservation. Equivalent or worse matrix outcomes would count against that advantage. Biotensegrity supplies a candidate architectural rationale for distributed load management, while established tissue mechanics provide the experimental basis. Evidence that auxeticity occurs, that ECM state regulates it, and that preserving it benefits the matrix represents separate levels of support. The contribution is therefore a testable preservation hypothesis, rather than the discovery of a new deformation phenomenon.