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hypotonia or venous and lymphatic disease and it was assumed that a previous varicose disease should exist for cellulite to appear. In most cases, the interstitial alterations of cellulite appear first and the varicose lymphatic pathology


or


manifests itself only later. However, the characteristic orange peel appearance of cellulite is either due to an increase in the fat or interstitial liquid content, or to the alteration and retraction of connective layers occurring in different times and manners3


. outward


Venous lymphatic stasis is the expression of


malfunctioning in the endocrine- metabolic regulation of the interstitial matrix or extracellular matrix (ECM). Today we know that cellulite is the result of a number of biochemical and metabolic


alterations that start on an interstitial matrix or ECM and connective structures level. The ECM is represented by a


complex structural entity that surrounds, nourishes, and furnishes support to all the cells. The main causes of alteration of the ECM are:


■ Reduction of the arteriolar microcirculation


■ Reduction of the cellular metabolism (increase free radicals)


■ Increase the flogistic process at the connective tissue ■ Alteration of the venous lymphatic system ■ Lipodystrophy evolution.


Background The term ‘cellulite’ was first used by Alquin and Pavot in France in 1920. Their insightful observations led them to associate this unaesthetic condition with a possible pathology accurately described a little later by Lagueze as a subcutaneous pathology characterised by ‘interstitial oedema associated with an increase in fat content’1 In 1940, Allen described cellulite mainly as a typical


.


lipoedema not accompanied by oedema in the foot. He further highlighted the prevalence of the metabolic alteration over venous-lymphatic impairment1


. In 1972, Braun and Falco made references to the


predominantly vascular disease describing it as a lymphoedema with various manifestations. Finally, in 1976, Reinharez, who had a deep knowledge


of the lymphatic system, described this disease as an endocrine-metabolic pathology having secondary vascular and lymphatic manifestations1 In 1978, Binazzi4


. , and later Sergio Curri5 40 ❚ — perhaps


the greatest specialist on microcirculation together with Joseph Merlen — histologically proved the


January/February 2015 | prime-journal.com


existence of microvascular alterations, dividing them into three groups: oedema, fibrosis, and sclerosis (hence the acronym EFP corresponding to oedematous fibrosclerotic panniculopathy). Recent discoveries have led to different evaluations


and, in 1997, Bacci et al described in Flebología hoy [Phlebology today] the conception of the cellulite disease as a ‘predominantly interstitial endocrine-metabolic pathology’1,6


. Today, we move our concept from Curri with the


oedematous fibrosus panniculophathy to a new concept of Bacci: female evolutive fibroedema.


Female evolutive fibroedema In the first instance, female evolutive fibroedema begins by initiating a functional alteration of ECM. Over time, there is a degenerative alteration of ECM with: ■ Diminishing arteriolar microcirculation (<T˚) ■ Increasing water in the fat tissue (lipoedema) ■ Endocrine metabolic alterations (periphery mesenchimopathy)


■ Decreasing venous lymphatic drainage (venous lymphatic oedema)


■ Inflammatory and fibrosis in connective tissue and fat tissue


■ Jellification of the ECM. The final complications include:


■ Surface hypoxia ■ Lipodystrophy ■ Tissular fibrosis ■ Sclerotic connective evolution. Observing the physiopathology of cellulite it is


understandable why treatments should be integrated and not limited to just adipose tissue treatments.


What’s new in adipose tissue? Adipose tissue (AT) has long been regarded as a resting tissue dedicated to energy storage and release. In recent years, this view has dramatically changed following new insights into the endocrine activity of adipocytes and the immunological functions of AT8


. The biology of AT is a


‘black hole’ in the field of dermatology, aesthetic medicine, and aesthetic surgery, although the demand for surgical procedures involving the manipulation of subcutaneous AT is rising every year (surgical removal, liposuction, and lipofilling procedures). Physicians working in aesthetic medicine and cosmetic surgery taking out AT and placing it elsewhere with rather crude technology should think carefully about the fate of the tissue and cells they manipulate.


Predisposition to cellulite There are many factors that have been shown to affect the development of cellulite and these include1


:


■ Family background, especially hereditary endocrine- metabolic syndromes, but also common nutritional deficiencies


■ Body structure, especially postural and spinal column alterations


■ Hormone imbalances in patients suffering from


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