This project aims to better understand the underlying mechanisms of endometriosis by studying the physiology of the uterine muscle, the myometrium. The disease is associated with myometrial hypercontractility, which is hypothetically linked to hormonal receptor overexpression, aberrant innervation, or muscular disorganization. To investigate this hypercontractility, we have combined functional and histological approaches. Ex vivo myometrial contractility is assessed using tissue slices from hysterectomy specimens subjected to oxytocin stimulation, a key regulator of uterine contractions. This method, which preserves the structural integrity of the tissue from the serosa to the endometrium, enables the analysis of peristaltic waves frequency, amplitude, nucleation sites, and propagation velocity. In parallel, immunohistochemical analyses of large myometrial sections are performed to map the distribution of oxytocin receptors along the serosa–endometrium axis. We find that contraction frequency in patients with endometriosis and/or adenomyosis is significantly higher than in controls. Organ-bath contractility involves the entire myometrial thickness from endometrium to serosa, in contrast with in vivo imaging observations (MRI/US) that usually highlight contractions close to the endometrium. We show that oxytocin can stimulate the nucleation of contractile waves close to the endometrium, correlating with high local oxytocin receptor expression at this site and supporting the hormonal regulation of wave directionality.

This study deepens our understanding of the pathophysiological mechanisms underlying uterine hypercontractility in endometriosis and adenomyosis, suggesting a direct role of oxytocin in reshaping the spatiotemporal dynamics of myometrial contractions.

Legend : Endometrium–myometrium junction in a patient with adenomyosis: endometrial glands invading the collagen-rich myometrium. SHG microscopy – Cochin Institute.

Lila Sarfati

Interfaces, in and out of equilibrium.

Interfaces between phases are ubiquitous in nature, from liquid drops to bird flocks. In equilibrium physics, surface tension is a three-in-one concept: it’s a force, it’s a thermodynamic free energy variation, and it’s what governs capillary relaxation. Out of equilibrium, no such synthesis exists. Forces can be defined, but thermodynamics does not apply. Some recent definitions even yield negative values of surface tension for a stable interface.  From the point of view of capillary relaxation, some progress can be made. My goal is to explain how to construct an evolution for the deformation of an interface between two phases in active systems that operate far from equilibrium.