The disease of cellulite

As a practicing dermatologist, not a day goes by in my office without a patient inquiring about the treatment of cellulite. Most are considering one of a plethora of novel cellulite oral or topical or mechanistic treatments that claim to improve the appearance of this dimpled, unattractive skin. I have observed the presence of cellulite, to a greater or lesser degree, on every woman in my office who is postpubertal. Then, can we in cosmetic dermatology call cellulite a disease? Perhaps cellulite is best characterized as a normal finding in mature women. Those women without cellulite are the oddities and perhaps have the actual disease! What exactly constitutes the etiology of this disease? Should we even be concerned in cosmetic dermatology about this so-called disease? These are the questions I would like to explore in this editorial. Cellulite, also known as adiposis edematosa, dermopanniculosis deformans, and status protrusus cutis, is perceived as uneven bumpy skin texture over the upper outer thighs, posterior thighs, buttocks, breasts, and upper arms.1 It seems to be found in areas where excess adipose tissue is deposited, although obesity is not necessary for the presence of cellulite. This appearance is thought to be caused by projections of subcutaneous fat into the reticular and papillary dermis. These herniations can be documented via ultrasound as low-density regions among the denser dermal tissue.2 The exact etiology of cellulite is unknown, but several theories deserve mention. The theories fall under several categories: vascular, structural, and inflammatory. Some investigators have postulated that cellulite is a degradation process initiated by deterioration of the dermal vasculature, particularly loss of the capillary networks.3 As a result, excess fluid is retained with the dermal and subcutaneous tissues.4 This loss of the capillary network is thought to be the result of engorged fat cells clumping together and inhibiting venous return.5 After the capillary networks have been damaged, vascular changes begin to occur within the dermis, resulting in decreased protein synthesis and an inability to repair tissue damage. Clumps of protein are deposited around the fatty deposits beneath the skin, causing an “orange peel” appearance to the skin as it is pinched between the thumb and forefinger. At this stage, however, there is no visual evidence of cellulite. The characteristic appearance of cellulite is only seen after hard nodules composed of fat surrounded by hard reticular protein form within the dermis. Ultrasound imaging of skin affected by cellulite at this stage reveals thinning of the dermis with subcutaneous fat pushing upward, which translates into the rumpled skin known as cellulite. Thus, this theory holds that hormonally mediated fat deposition, fat lobule compression of capillary vasculature, decreased venous return, formation of clumped fat lobules, and deposition of protein substances around clumped fat lobules lead to the appearance of cellulite. Cellulite treatments employing vascular manipulations are based on this theory. Some investigators who espouse the structural theory have observed that cellulite is more common in overweight and obese women. They believe that cellulite is caused by the presence of copious fat lobules within the subcutaneous tissue encased in fibrous septa with dermal attachments. These fibrous attachments surrounding abundant fat lead to the rumpled appearance of the skin, characteristic of cellulite. Thus, weight loss, which reduces the size of the fat lobules, improves the appearance of cellulite. Improvement can also be achieved with exercise, as improved muscle tone creates a better foundation to support the overlying fat. This structural theory of cellulite is the least commonly accepted at the time of this writing, but treatment is based on exercise and weight loss. The last theory on the etiology of cellulite holds that it is an inflammatory process resulting from collagen breakdown in the dermis providing for the subcutaneous fat herniations seen on ultrasound. The onset of cellulite with puberty and menstruation has caused some researchers to evaluate the hormonal changes necessary for sloughing of the endometrium.6 It appears that menstruation requires the secretion of metalloproteases (MMP) such as collagenase (collagenase-1, MMP-1) and gelatinase (gelatinase A, MMP-2).7 The endometrial glandular and stromal cells secrete these enzymes to allow menstrual bleeding to occur. Collagenases cleave the triple helical domain of fibrillar collagens at a neutral pH and are secreted just prior to menstruation. However, the collagenase may not only break down the fibrillar collagens present in the endometrium, but also in the dermis. Furthermore, gelatinase B is produced by stromal cells or mast cells during the late proliferative endometrial phase and just after ovulation. Gelatinase B is associated with an influx of polymorphonuclear leucocytes, macrophages, and eosinophils, which also contribute to inflammation.8 A marker for this inflammation is the synthesis of dermal glycosaminoglycans, which enhance water binding, further worsening the appearance of the cellulite through swelling. The presence of these glycosaminoglycans has been observed on ultrasound as low-density echoes at the lower dermal/subcutaneous junction.9 The secretion of endometrial collagenase to initiate menstruation also provides for collagen breakdown in the dermis.10 With repeated cyclical collagenase production, more and more dermal collagen is destroyed, accounting for the worsening of cellulite seen with age. Eventually, enough collagen is destroyed to weaken the reticular and papillary dermis and allow subcutaneous fat to herniate between the structural fibrous septa found in female fat. Obviously, if more subcutaneous fat is present, more pronounced herniation can occur. At present, this theory of chronic inflammation, resulting in cellulite formation, has the most scientific data and I personally agree with this hypothesis. Thus, trying to treat cellulite is much like trying to ignore the normal female physiology that allows for the continuation of the species. Why should women be depressed about something that is a normal part of female anatomy? Why should attention be focused on preventing or eliminating the inevitable? Perhaps cosmetic dermatology should take a closer look at how we define a disease. Can a condition be characterized as a disease if the majority of the population possesses this finding? I believe the answer is emphatically “no.” Cellulite is not a disease.