Mechanism of action of stem cells in vulvar lichen sclerosus
The Liquenia® protocol is not empirical—it has a documented biological basis. This page explains why adipose tissue-derived mesenchymal stem cells are biologically consistent with the pathophysiology of VLS.
What happens in vulvar tissue with VLS
To understand why the Liquenia® protocol acts on VLS, it is first necessary to understand what is happening in the vulvar tissue affected by the disease.
VLS is an autoimmune disease. The immune system generates a chronic inflammatory response against vulvar tissue, producing several effects at the tissue level:
Chronic inflammation with T-lymphocyte infiltrate
Autoreactive T lymphocytes continuously attack vulvar tissue. This chronic inflammation is the direct cause of symptoms and progressive tissue damage.
Fibrosis and loss of tissue architecture
Chronic inflammation activates fibroblasts, which produce excess collagen. The result is fibrosis—the vulvar tissue loses its normal architecture and becomes stiff, thickened, and less elastic.
Epithelial atrophy
The vulvar epithelium progressively thins, losing the layers that normally protect it. The skin becomes fragile and vulnerable.
Impaired vascularization
Chronic inflammation alters the microvasculature of vulvar tissue, reducing the supply of nutrients and oxygen.
The mechanism of the stromal vascular fraction
The stromal vascular fraction (SVF) of adipose tissue contains a heterogeneous population of cells, among which **mesenchymal stem cells (MSCs)** stand out. These cells are the ones with therapeutically relevant effects in the context of VLS.
Anti-inflammatory effect
MSCs secrete soluble factors—anti-inflammatory cytokines such as IL-10 and TGF-β—that inhibit the activation and proliferation of T lymphocytes involved in the autoimmune response in VLS. This directly reduces the local inflammatory burden, acting on the mechanism that causes tissue damage—not only on its consequences.
Immunomodulatory effect
MSCs modulate the local immune response in a more sophisticated way than simple suppression. They promote the differentiation of regulatory T lymphocytes (Treg), which have a protective function on the tissue. This effect is qualitatively different from that of corticosteroids, which suppress the inflammatory response more non-specifically.
Regenerative effect
MSCs stimulate the proliferation of native fibroblasts, the synthesis of high-quality collagen (as opposed to the disorganized fibrotic collagen in VLS), and tissue neovascularization. They actively contribute to repairing the tissue architecture altered by the disease.
The role of nanofat
Nanofat is mechanically processed adipose tissue: a fluid fraction that preserves the growth factors present in fat, as well as regenerative mediators derived from adipose cells. Unlike SVF, nanofat does not provide a concentrated cellular fraction, but it does contribute to the protocol’s reparative effect through other mechanisms.
The growth factors present in nanofat—VEGF, HGF, IGF, among others—directly stimulate cell proliferation, angiogenesis, and repair of damaged tissue. In the context of VLS, nanofat acts mainly on restoring vascularization and the structural quality of vulvar tissue.
Its effects add to those of SVF—anti-inflammatory and immunomodulatory—creating a multi-mechanism approach to the pathophysiology of VLS:
The protocol as a sum of effects:
SVF (anti-inflammatory + immunomodulatory + regenerative) + nanofat (regenerative + angiogenic + tissue-repair) = a multi-mechanism approach to the underlying mechanisms of VLS.
What biopsies confirm
The protocol’s biological consistency is confirmed in histological data. Comparative biopsies performed before the procedure and at 3 months show changes consistent with the expected mechanism of action:
> Reduction of inflammatory infiltrate in the dermis
> Increase in epithelial thickness
> Improvement in the architecture of dermal collagen
> Greater tissue vascularization
These objective histological changes are what distinguish the Liquenia® protocol from approaches that only assess symptom control without documenting what happens in the tissue.