• General Information

WHAT IS CELLULITE?

Cellulite consists of the appearance of orange peel skin localised most frequently on the buttocks and top outside and back of thighs, (1) (Avram). As one ages, cellulite also settles on the inside thigh and arms. It could actually appear on any part of the body where there is a presence of hypodermic adipose tissue, so it could appear on the chin, lower abdomen, back, waist and the stomach area.

It cannot be considered a disease but, despite this, it is an aesthetic problem that affects 90% of women throughout the world. Giving it major relevance within the universe of medical-aesthetic treatments.

Its appearance is related to the oestrogenic essence of the post-pubescent female since it is not common among males, except in cases where an androgen deficiency disorder is present, such as hypogonadism, post-castration syndromes or prostate cancer treatments using therapy based on oestrogenic derivatives.

Cellulite developed by Caucasian women is more severe and frequent than among Asian women.

There is no sole definition of the reason of its appearance, although it is generally accepted that cellulite stems from four basic causes:

According to how its pathophysiology is understood, it acquires different denominations such as dermopanniculosis deformans, adiposis edematosa or gynoid lipodystrophy.

Cellulite treatment starts with approaching the possible aggravating factors, the mechanical and physical treatments, pharmacological treatments, laser and radiofrequency.

Ultrasound has shown that the dermis proper of cellulite is characterised by areas of soft tissue with low ultrasound density between areas of denser ultrasound tissue. The skin architecture of the fat lobes in the female hypodermis and the fibrous septa that separate them are designed perpendicular to the skin. This allows for protrusion of the fat lobes over the dermo-hypodermic junction, preventing the dermis subjected to more tension from retaining the pressure and displaying protrusions of the fat tissue (visible to the naked eye) in the dermo-epidermal junction.

These protrusions are not found in male skin given that the disposition of its septal connective tissue trabeculae is mesh-shaped and retains the pressure from the fat lobes better. Therefore, the dermo-epidermal junction is smoother and more homogeneous. (Nürberg and Müller) (2)-

Source: Journal of Cosmetic Laser Surgery, 6:181-1859, 2004 - Cellulite: A Review of Its Physiology and Treatment by Mathew M. Avram, MD.

However, other authors (Pierard, (3)) have found no clinical correlation between the presence of these protrusions of fat lobes against the dermo-epidermal junction with the appearance of visible cellulite; relating its appearance more with the presence of the vertical lengthening of these hypodermic connective fibres that lead to their weakening and elongation and allowing for visible herniation of the fat.

On the other hand, according to the theories of Curry (4 and 5), as well as Rossi and Vergnanini (6), an affectation of the capillary microcirculation is produced (predominantly in the pre-capillary arteriolar sphincter as a consequence of hyperpolymerised glycosaminoglycan (GAGs) deposits in the external area of the capillaries and in the extracellular matrix between the elastin and collagen networks. This strangulation caused by the perivascular environ, produces an increase of the precapillary pressure with an increase in permeability of the capillary and vernular structure and the consequential retention of fluids in the extracellular space of the dermis and the hypodermis between the lobes and the connective septa.

GAGs are hyhdrophilous, they increase the interstitial pressure and attract more water to the extracellular space, which worsens the oedema. Finally, the high grade of oedema causes vaso-compression of the micro-vascularisation with static vessels, decrease in venous return and tissue hypoxia.

The situation of atmospheric hypoxia together with the depositing of GAGs in the extracellular matrix and the collagen and elastin networks triggers neocollagenesis and neovascularisation.

A lipogenesis, possibly stimulated by oestrogens, prolactin and carbohydrate-rich diets together with lipolysis due to hypoxia lead to adipocyte hypertrophy. Therefore clusters of hyperplasic and hypertrophic adipocytes are produced around the highly fibrous conjunctive septa. Hypoxia, vascular congestion and oedema affect the most superficial adipose tissue as well as the base of the dermis, making the problem visible.

There is also an interpretation that proposes inflammatory components, Kligman (7) as a consequence of finding chronic inflammatory cells, macrophages and lymphocytes in biopsies of cellulite affected skin septa.