Cellulite (also known as gynoid lipodystrophy, adiposis edematosa, panniculosis deformans, nodular liposclerosis, edematous fibrosclerotic panniculopathy, local lipodystrophy, and status protrusus cutis) is a complex cellular dystrophy of dermal and subcutaneous tissue.1
Affected skin has a dimpled and/or nodular appearance, described as resembling an orange peel, cottage cheese, mattress or tufted cushion.3
It is most commonly found on the thighs, hips, buttocks, and, to a lesser extent, the stomach and posterior arms.
There are no epidemiological data on the incidence or prevalence of cellulite, although it is estimated to affect between 80% and 98% of postpubertal women.2
As such, it may be more appropriate to conceptualize cellulite as a female secondary sex characteristic.2
An estimated 2% men are affected.3
That cellulite occurs in nearly all women after puberty suggests an evolutionary significance. There is recent evidence that gluteofemoral subcutaneous adipose tissue has cardioprotective effects. Adipose located on the thighs and buttocks is inversely related to atrial stiffness and the ability of this tissue to entrap and store fatty acids and lipids, preventing their deposition into ectopic sites such as the liver, pancreas, and muscle.5
Cellulite may also play a role in energy homeostasis and insulin sensitivity via localized production of adipokines.8
Little data exist on racial/ethnic distribution of cellulite, although Caucasian women tend to be more affected than Asian women.2
The condition is usually asymptomatic and not associated with morbidity or mortality. It is, however, one of the most common causes of cosmetic concern among women.2
Patients present with complaint of rippling, dimpling, or irregular contour of the skin most commonly on the hips, thighs, and buttocks.
FIGURE 6.2.1 Pinch test. A, In the female there are fat cell conglomerations in the upper part of the subcutis (standing fat chambers) and papillae adiposae. B, In the male there are only folds and furrows produced.
When first described by Albert and Paviot in 1920, cellulite was proposed to be a noninflammatory dystrophy of mesenchymal tissue, wherein defects in water metabolism led to saturation of adjacent tissues by interstitial fluid.2
It is now thought that cellulite is caused by a complex interplay of endocrine-mediated dermal and subcutaneous inflammatory events, microvascular dysfunction, and connective tissue fibrosclerosis.2
Recent studies show a correlation between cellulite and the insertion/deletion polymorphism in the HIF1A gene encoding for angiotensin 1-converting enzyme. Women with the D allele of the gene produce increased amounts of angiotensin II in their subcutaneous adipose tissue, causing decreased local blood flow and reduced expression of adiponectin.5
Women with the rare mutant T allele of the gene are protected against the development of cellulite owing to their blunted physiological fibroinflammatory response.18
From a genetic standpoint, a 2-hit hypothesis is then proposed for the development of cellulite: the first hit, a carriage of the D allele and localized adipose tissue hypoperfusion, and the second hit, a microenvironment of proinflammatory cytokines, decreased adiponectin expression and formation of collagen strands.5
Microvascular dysfunction in the subcutaneous tissue results in hypoxia, inflammation, and adipose tissue degeneration, followed by septal capillary neoformation and increased collagen synthesis and eventual fibrotic response around adipocytes with formation
of thick septae.2
Biopsies of cellulite show a mild inflammatory infiltrate of macrophages and lymphocytes and microhemorrhages in fibrous septae, which are thought to result in dermal atrophy. Herniated adipocyte lobules cause sustained mechanical tensions and prevent venous return, further contributing to hypoperfusion.21
This partially explains the observation that a sedentary lifestyle with prolonged periods of sitting or standing, and thus impediment of normal blood flow, is correlated with higher severity of cellulite.2
FIGURE 6.2.2 Hexsel cellulite severity scale.
FIGURE 6.2.3 Cellulite anatomy. (Courtesy of Designua/Shutterstock.com.)
Premium Wordpress Themes by UFO Themes
The postpubertal onset of cellulite denotes the significant role of sex hormones in the pathogenesis of the condition. Menstruation requires endometrial secretion of the metalloproteases (MMPs), collagenase, and gelatinase to cleave triple helical domains of fibrillary collagen and water binding of glycosaminoglycans (GAGs), respectively.21
MMPs are also secreted in the dermis, and their cyclical secretion during monthly menstrual cycles allows for progressive dermal collagen destruction, adipose herniation, and worsening of cellulite with age.1
Estrogen activates fibroblasts and increases adipocyte response to anti-lipolytic alpha-2 adrenergic receptors and promotes GAG synthesis, which results in increased interstitial osmotic pressure and fluid retention.5
17-β-Estradiol, specifically, stimulates replication of adipocytes.2
During pregnancy, increases in prolactin, insulin, and overall fluid volume promote cellulite lipogenesis and fluid retention and cause the worsening appearance of cellulite.2
Testosterone, in contrast, stimulates connective tissue, resulting in decreased adipocyte protrusion through septae, and fewer dimples on the skin surface. This supports why so few men develop cellulite and explains the phenomenon whereby men with prostate cancer on estrogen therapy, develop cellulite.17
WordPress theme by UFO themes