Abstract

Objectives: Cellulite is a dimpled, lumpy skin appearance in the gluteofemoral body area, occurring almost exclusively in females. This chronic skin condition is widespread and affects more than 85% of females over 20. Cellulite does not necessarily correlate with BMI's onset can be seen as early as during puberty. It does not demonstrate a significant association with lipedema, another GF-related disorder. Still, its manifestations are much more severe, with a reduced incidence rate and unknown pathophysiology, apparent mostly as a dramatic expansion of the subcutaneous white adipose tissue. Introduction: Various pathophysiologies of cellulite have been proposed in the past. However, none of these proposed mechanisms can explain the most pronounced morphological alterations observed in the cellulite skin, namely, the distinct protrusions of the underlying adipose tissue into the dermis. Materials / method: Pronounced protrusions of adipose tissue into the dermis can be caused either by reduced levels of adhesion between skin and WAT on the dermal–hypodermal junctions or by special properties of the superficial adipose tissue in cellulite skin, allowing its higher invasiveness. Here, we analyze recent results concerning the superficial adipose tissue in humans and the new morphological findings in cellulite skin and underlying adipose tissue. We propose a new pathophysiology of this skin condition, which can explain the appearance of WAT protrusions in the dermis. Results: Metabolic endotoxemia is a widely accepted pathophysiological factor in generalized adiposity and diabetes. However, the accumulation of LPS within a specific WAT depot has so far not been considered as a possible pathophysiological mechanism triggering localized WAT modifications. Still, it may very well be involved in such conditions as lipedema or cellulite. Here, we propose that the gfWAT depot provides conditions for local activation of TLR4 receptors. This makes this tissue more sensitive to low doses of LPS in gfWAT and will induce low-grade inflammation and promote fibrosis. Conclusion: Whereas such low-grade gfWAT-specific endotoxemia should be a common effect leading to its low-grade inflammation accompanied by fibrosis and enhanced protrusions into the dermis, further increase of endotoxemia level in gfWAT must lead to the uncontrollable expansion of this tissue observed by lipedema. Also, I propose a new scheme of treatments based on the new physiopathology.