Cellulite formation stages Stage 1: The first events in cellulite formation are invisible, occurring at the cellular and molecular level. A dermal deterioration is the hallmark of the first stage of cellulite formation. Blood vessel integrity breaks down, with the upper dermal region showing a loss of capillary networks.
This is not unlike the deterioration associated with sun damage. Fat cells become engorged with lipid, often swelling to two or three times their original size, and begin clumping together. An excess of fluid is retained in the dermal and sub dermal regions.
Fluid accumulation is most likely due to the capillary breakdown, but whether this is a cause or an effect of the disturbed fat metabolism is a subject of debate. Stage 2: In the second stage of cellulite development, the tissue at the sub dermal and dermal levels has deteriorated; blood vessels in the afflicted area are disrupted.
Some regions have normal microcirculation while adjacent regions can have markedly reduced blood flow. Fat cells engorged with lipid, clump together in the skin fat layer. This exacerbates the microcirculation problem, with the blood vessels being pushed away by the regions rich in fat deposits. In addition, fluids tend to accumulate, increasing the problem in the sub-surface region.
In general, a surface lumpiness or unevenness can be seen. Stage 3: This stage is a continuation of the process in stage 2. Vascular deterioration begins to effect changes in the dermis, resulting in a less active dermal metabolism. Treatment options for lipedema may include:. Cellulite is a skin condition in which fat cells push against the skin while connective tissue pulls them down, causing a dimpled appearance in the skin. Cellulite commonly appears on the thighs, buttocks, and other areas where there may be a higher accumulation of fat cells.
Generally, these dimples can cause the skin to appear as bumpy or uneven, although this often depends on how shallow or deep the dimples are. The more fat you have in an area, the more prominent it can be, but even thinner individuals can have cellulite. Treatment options for cellulite may include:. Lipedema and cellulite are two separate health conditions, both of which can cause noticeable changes to the appearance of the skin. Whether you call them fat ankles, cankles, or just swollen, they can be typical for you or a serious health condition.
We explain the causes, risks…. Dry brushing can help get rid of dead skin cells and stimulate blood flow. But what about reducing cellulite? The structural unit of adipose tissue is an adipocyte. These cells are dispersed within a scaffold consisting of collagen fibers.
In addition to adipocytes, the adipose tissue consists of preadipocytes, fibroblasts, leukocytes, macrophages, endothelial cells and myocytes. The presence of these cells suggests that body fat performs a complex and heterogeneous function beyond that of lipid storage. Cellulite should not be confused with obesity, in which a gain in adipose tissue mass results from an increase in adipocyte cell size and number.
The primary function of the adipocyte is associated with the metabolism of fatty acids. They also have a lot of endocrine functions [ 16 ]. Emanuele et al. However, plasma adiponectin levels did not differ between women with and without cellulite, what suggests that this molecule may act as a local paracrine factor that influences the appearance of the skin [ 18 ].
Other studies support the thesis that endocrine function of subcutaneous adipose tissue may functionally affect the subcutaneous vascular and lymphatic circulation and possibly influence the formation of cellulite [ 19 ].
Adipocytes are equipped with a number of specialized receptors enabling them to interact with the endocrine system [ 6 , 16 , 20 ]. Disorders of the adipocyte endocrine function correlate with the current state of the metabolism.
Endocrine system failure is observed both in the case of excess adipose tissue insulin resistance, diabetes , and its deficiency malnutrition [ 6 , 20 ].
Impaired secretion and production of adipocytokines results in the disruption of homeostasis. Excess body fat is associated with insulin resistance, hypertension and an increased risk of atherosclerosis. These factors directly affect the vascular dysfunction, not only regarding cardiovascular events. Adipocytes become hypertrophic when adipose tissue is in excess, and progressive reduction of micro-circulation is observed in the local area as the individual cells mutually constrict each other.
It is believed that the coexistence of the aforementioned factors can play a role in the pathogenesis of lipodystrophy [ 16 , 21 ]. Contemporary literature attributes a key role in the pathogenesis of many diseases to the dysfunction of the vascular endothelium [ 22 ]. This single layer of cells lining the inside walls of blood vessels is considered to be a separate organ because of its endocrinal, vasodilatory and vasoconstrictive attributes.
Endothelial dysfunction has long been recognized as an independent risk factor for the cardiovascular disease, cancer and type II diabetes. Endothelial damage is regarded as a pathomechanism in the case of insulin resistance, in which damage results in the production of reactive oxygen species and the excessive glycosylation of proteins, thus reducing the availability of nitric oxide, and increasing the production of growth factors and pro-inflammatory cytokines [ 22 ].
A similar situation has been speculated in the case of cellulite. A local inflammatory process dependent on macrophages and Th1 cells can influence the endothelial dysfunction in obese people experiencing GLD. In obese people, increased recruitment of M1 macrophages has been demonstrated [ 23 ]. A large number of them are present in the adipose tissue of obese people.
It has also been demonstrated that a high level of IL-6 is an independent risk factor for cardiovascular events [ 8 ]. A correlation between obesity, insulin resistance, local inflammation and endothelial dysfunction is possible. As these factors have been found to co-occur in cellulite, it is possible that they share a similar pathology with that of the vascular endothelium [ 24 , 25 ].
It is sensitive to the concentration of oxygen in the cellular environment. The HIF occurs in all tissues of the human body.
It regulates gene expression in response to hypoxia, resulting in counteracting the harmful effects associated with lack of oxygen. During hypoxia, the expression of the HIF-1 gene stimulates the production of the GLUT 1 protein, erythropoietin, transferrin and vascular endothelial growth factor VEGF , which enable the cells to prepare for hypoxia [ 27 ]. This results in the stabilization of HIF1A subunits and the activation of hypoxia-inducible gene expression.
An increased expression of HIF-dependent protein-1 has been observed in many malignant tumors [ 23 ]. Its expression is associated with a rapid and uncontrolled proliferation of cancer cells and insufficient neoangiogenesis [ 27 ]. Adipose tissue expansion in response to increased caloric intake is regarded as a potent stimulus to HIF1 gene expression, which stimulates a fibrogenic response typical for cellulite.
Ischemia and hypoxia also play a role in cellulite. Microcirculation disorders, local inflammation, endothelial dysfunction and fibrosis of subcutaneous tissue all occur as responses to chronic hypoxia. In fat tissue, HIF-1 expression has been found to activate fibrosis and local inflammation. T-allele of polymorphism for HIF1A reduces the activity of the HIF-1A factor in patients, and one study found that women presenting this particular polymorphism did not develop cellulite, or if they did, it was at a low level [ 22 ].
This relationship illustrates the connection between GLD and HIF1 factors, and represents another link between local micro-circulation disorders and the development of lipodystrophy. Adiponectin is a peptide that belongs to a group of adipocytokines, molecules secreted by adipocytes, and serves a vasoprotective and antiatherogenic agent. In addition, adiponectin protects the vascular endothelium and facilitates the proper metabolism of glucose and lipids. Reduced concentrations of this peptide are observed in obesity, diabetes, hypertension and coronary heart disease, while high concentrations have been documented in cases of longevity.
In addition, a close relationship has been noted between low concentrations of adiponectin, insulin resistance and the risk of developing type 2 diabetes [ 28 ]. Adiponectin is known to not only have strong antiatherogenic properties, but also to act as a vasodilatory and anti-inflammatory factor. Low levels of this protein correlate with impaired vasodilation, thus impeding microcirculation [ 28 — 30 ].
These findings imply a probable link between low concentrations of adiponectin and the development of cellulite. Leptin is also synthesized by adipocytes. The worldwide obesity problem is steadily increasing, which necessitates the search for new targets to fight the accumulation of excess fat also called adipose tissue.
Interestingly, it was recently discovered that apart from normal white adipose tissue WAT , which is responsible for storing fat in oil droplets, adult humans also possess a pool of brown adipose tissue BAT. The purpose of this BAT is to burn fat into heat. It was long thought that BAT only exists in newborns as they are unable to produce body heat through shivering.
However, novel scientific findings have shown that white fat cells are able to transform — upon activation — into brown-like fat cells which are also able to burn lipids into heat. Brown adipocytes fat cells constitute the BAT. In contrast to white adipocytes, brown ones contain much smaller fat droplets and a much higher number of mitochondria, the organelles that generate energy for the cell.
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