An article by Bryton et al., published in November 2025 in *Scientific Reports* (Nature Portfolio), begins by decisively challenging the classical paradigm of endolymphatic hydrops, proposing that its pathophysiological basis lies in active epithelial hyperplasia rather than in increased hydrostatic pressure.
Using post-mortem human histology, 3D reconstructions, machine-learning-assisted cell quantification and immunohistochemistry, the authors demonstrate a marked increase in the number of cells in Reissner’s membrane and the sacular membrane, with no signs of mechanical distension or rupture.
This hyperplasia develops at an early stage and appears to be a compensatory response to the functional loss of the endolymphatic sac, a key structure in the homeostasis of the inner ear.
The newly formed cells continue to express ion transport proteins, suggesting that their physiological function is preserved.
This new model redefines hydrops as a biological and dynamic phenomenon, with the potential to transition from adaptation to maladaptation.
Future implications point towards new therapeutic approaches, focused on modulating epithelial regeneration and preventing pathological remodelling, rather than simply reducing endolymphatic “pressure”.
