Cellulite affects millions of women around the world. All media outlets that target the young female population concentrate heavily on this problem and its various means: numerous methods and procedures, all of which achieved a short-term triumph before being rendered ineffective. In the article on estet-portal.com you will learn about the etiopathogenesis of cellulite in order to select successful strategies in the treatment of cellulite.
- Excessive hydrophilia as a cellulite trigger
- Impaired microcirculation in the pathogenesis of cellulite
- Conclusion
Excessive hydrophilia as a cellulite trigger
Back in 1964, the phenomenon of hyperpolarization of acid mucopolysaccharides in the connective matrix of the subcutaneous adipose tissue of patients suffering from cellulite was described. Thus the reason was explained an abnormal increase in tissue hydrophilia, provoking chronic edema, leading to fibrosclerosis. This observation has had a lasting impact on therapeutic approaches, justifying the topical or mesotherapeutic administration of hyaluronidase and other agents known to have a lytic effect on proteoglycans.
Using electron microscopy, we examined the dermis of the skin, covering the areas of adipose tissue affected cellulite; there was a marked increase in the presence of glycosaminoglycans, signs of fibroblast activation, changes in the walls of microvessels, as well as a rarefaction of subepidermal collagen and elastic fibers. This histochemical scenario is indicative of an abnormal connective response that, due to fluid retention in the interstitial matrix, can lead to the deposition of new collagen in the subcutaneous tissue.
Impaired microcirculation in the pathogenesis of cellulite
The most popular theory in Europe explains cellulite as a consequence of a primitive dysfunction of tissue microcirculation. Indeed, European researchers have made a significant contribution to the development of this theory.
According to Binazzi, the initial stage is often associated with obesity and is clinically characterized by uneven skin surface of the buttocks, thighs, abdomen and shoulders, the so-called "mattress effect". Histological examination reveals only extreme variability in adipocyte size and shape (anisopoikilocytosis), as well as dermal edema, lymphatic dilation, and areas of follicular hyperkeratosis (orange peel).
The next stage is distinguished by the presence of nodular rashes on palpation, which are mobile and painful, with a diameter of 1 to 5 & ndash; 6 mm; histological sections indicate deep damage to the subcutaneous tissue with connective ligaments surrounding fat lobules forming nodular neoplasms that become sclerotic; hemorrhagic or thrombotic vascular changes are also observed. Some authors link these regressive processes in a pathogenetic interpretation that identifies primary movements in violation of fragile homeostasis at the microcirculation level.
Methods for the prevention and treatment of cellulite.
Recent advances have made it clear that the endothelium plays a key role in microcirculatory homeostasis. The endothelium does not simply perform the mechanical role of an endoluminal covering; it also modulates the exchange of blood and tissue through the complex action of biosynthesis, reminiscent of the diffuse function of the glands, regulates the balance between many phenomena (pro- and anticoagulant, fibrinolytic and antifibrinolytic, vasodilatory and vasoconstrictor).
Morphological features of subcutaneous fat:
- capillary network with very closely spaced
branches, in close proximity to adipocytes, reducing the "diffusion space"; to a minimum;
- absence of arteriovenous anastomosis: this leads to the conclusion that continuity of adipocyte perfusion is a condition that should not be sacrificed;
- branches connecting the arteries and veins of the adipose tissue with the choroid plexuses of the dermis and muscle tissue: they form cylindrical units located perpendicular to the surface of the skin and extending from the latter to the hypodermis. This justifies the fact that the microcirculatory deficit in panniculopathy is often associated with changes in blood flow extending to the skin and regional musculature. The presence of estrogen receptors in endothelial cells and smooth muscle explains the functional differences in the female microcirculation, especially in relation to vascular tone and permeability.
The causative factor is defined as a chronic maldistribution of the microcirculation, which in turn is due to a primitive defect in the arterial device that modulates blood flow. The consequences of this condition, which can be attributed to the field of hypotonic phlebopathy (preclinical stage of venous insufficiency) are as follows:
- slow blood circulation;
- erythrocyte sediment phenomena;
- disturbance of hydrostatic capillary balance;
- decrease in parietal and tissue oxidation;
- endothelial injury (endothelial edema, microhemorrhage);
- abnormal capillary-venular permeability;
- increase in fluid hydrostatic pressure and protein content;
- Recurrent episodes of interadipocytic edema.
Adipocyte injury is first manifested by anisopoikilocytosis, followed by plasma membrane ruptures and leakage of lipid material. The thin weave of fibrils that serve as a scaffold for the fat lobule, covering each individual cell, thickens due to hypoxia and oxidative stress. Stripes of young connective tissue appear, forming a lobule, surrounding accumulations of degenerative fat cells. Subsequently, the micronodules formed in this way tend to coalesce due to further overlay of collagenous material which becomes sclerotic, leading to the formation of palpable macronodules that cause uneven skin surface.
Effective cosmetic techniques against cellulite.
Two German physicians, Nürnberger and Müller, citing histological findings from a wide range of cases (150 cadaveric specimens and 30 living specimens), deny any evidence of edema or fibrosis. In fact, they attribute the appearance of skin irregularities in typical female areas to a combination of two causative factors:
- excessive lipid deposition (without obesity there is no cellulite);
- a peculiar architecture that in women characterizes the subcutaneous tissue in these areas, where fibrous branches perpendicular to the surface of the skin divide the voluminous lobules into rectangular areas; their tops are pressed against the dermis and pushed outward in the form of "fat lobes".
Thus, the dermo-subcutaneous border in the "cellulite areas" characterized by a "hill" profile, which, in the case of perfect normality, can be confirmed with a "pinch test".
In women who have thickening of the subcutaneous panniculus in areas typical of gynoid obesity, the lobules become enlarged. They are held laterally in bands, but in the center they merge into the dermis with hypertrophied fat lobes, creating an unattractive alternation of bulges and depressions, which at first appear only when standing upright, but become subsequently also visible when lying down.
On the other hand, in the male subcutaneous tissue, the streaks have a different direction, crossing over and thus forming smaller polygonal lobules which, even in cases of excessive lipid accumulation, do not tend to protrude towards the dermis. In hypogonadal men, adipose tissue assumes female morphology, demonstrating that androgen activity is a causal factor in any gender differences. Numerous reviews on the subject of cellulite have confirmed the opinions of Nuremberger and Müller.
Among them, Marenus suggested that the projection of the fat lobes towards the dermis is caused by the degeneration of the collagen component as a result of the action of certain proteases.
Rosenbaum and others also noted individual variability in addition to gender differences. The subcutaneous tissue in women with cellulite is characterized by a more uneven and disturbed subdermal layer, which is a factor that allows fat lobules to protrude.
Furthermore, he identified two interesting pieces of data: the first is related to the lack of a direct correlation between body mass index (BMI) and the appearance of skin surface irregularities: among women whose BMI exceeds 30, one can distinguish women without signs of cellulite and women who suffer more or less seriously from this dysmorphism. This demonstrates that factors other than localized excess adipose tissue play a role in the dislocation of fatty herniations. The second part of the data relates to the fibrous component of the subcutaneous tissue affected by cellulite: MRI showed that its overall size did not increase, but, on the contrary, apparently decreased significantly compared to the control. The authors therefore identify one of the pathogenic elements of cellulitis as constitutional thinness and laxity of the fibrous interlobular ligaments.
Simply put, based on a study of 39 autopsy specimens, although they confirmed the presence of fat lobes in the female, it was concluded that these masses were too small to produce the rough combination of bulge and depression typical of cellulite. However, this case may be associated with the progression of obesity, which causes stretching of the interlobular branches; some of them will undergo a retraction phenomenon (due to reactive thickening and the appearance of myofibroblasts), while others will suffer partial tears similar to stretch marks, causing irregular protrusions of the fat lobules. This observation prompted the authors to try a therapeutic approach with retinol, although it only gave moderately positive results.
Conclusion
Most recent research tells us that in obese individuals, among the functional changes that adipocytes experience when they become hypertrophic is an increase in the release of phlogogenic cytokines. This causes systemic effects and at the same time causes in a seemingly "normal" adipose tissue as a whole macrophage infiltration, the size of which is proportional to the average adipocyte volume. Consequently, obesity entails the activation of biochemical and cellular mechanisms of a phlogistic nature at the regional level.
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