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Cellulite Open Access to Scientific and Medical Research DOI Journal name: Clinical, Cosmetic and Investigational Dermatology Article Designation: REVIEW Year: 2017 Volume: 10 Clinical, Cosmetic and Investigational Dermatology Dovepress Running head verso: Friedmann et al Running head recto: Cellulite open access to scientific and medical research DOI: http://dx.doi.org/10.2147/CCID.S95830 Open Access Full Text Article REVIEW Cellulite: a review with a focus on subcision Daniel P Friedmann1 Abstract: Cellulite is an alteration in skin topography most often found on the buttocks and Garrett Lane Vick2 posterolateral thighs of the majority of postpubertal females. This article aims to review the Vineet Mishra3 background, potential pathophysiology, and potential treatment options for cellulite, highlighting subcision as an ideal therapeutic option for this cosmetically distressing condition. 1Westlake Dermatology Clinical Research Center, Westlake Keywords: gynoid lipodystrophy, fibrous septae, radiofrequency, vacuum-assisted subscision Dermatology & Cosmetic Surgery, Austin, 2Department of Medicine, 3Division of Dermatology and Introduction Cutaneous Surgery, The University of Cellulite is a descriptive term used to characterize the cosmetically distressing, altered Texas Health Science Center at San Antonio, San Antonio, TX, USA (eg, dimpled, padded, peau d’orange) topography of skin located most commonly on the outer thighs, posterior thighs, and buttocks of the majority of postpubertal females.1 First described in the early 20th century, it has been referred to by several synonyms, including gynoid lipodystrophy, nodular liposclerosis, edematofibrosclerotic pannicu- lopathy, panniculosis, adiposis edematosa, dermopanniculosis deformans, and status protrusus cutis.2–4 Many modalities, including subcision, have been purported to treat cellulite. This article aims to review the background, potential pathophysiology, and potential treatment options for cellulite, highlighting subcision as an ideal therapeutic modality for this condition. Epidemiology Despite its high prevalence (80%–90%) in postpubertal female patients of all races, little epidemiologic data on its exact prevalence, incidence, and associating factors have been published.5 Cellulite may worsen during high estrogen states, including pregnancy, nursing, and chronic use of oral contraceptives. Although diet, exercise, and lifestyle, however, do not appear to be associated with its development, weight gain and obesity can worsen the appearance of existing cellulite. Cellulite in male patients is rare and a product of androgen deficiency secondary to castration, hypogonadism, Klinefelter’s syndrome, or estrogen therapy for prostate cancer.3 Correspondence: Daniel P Friedmann Westlake Dermatology Clinical Research Center, 8825 Bee Cave Rd, Ste 100, Pathophysiology Austin, TX 78746, USA Cellulite is multifactorial, with sexual dimorphism of subcutaneous connective tissue, Tel +1 512 615 3193 the effects of localized increases in tissue tension, and local circulatory and inflam- Fax +1 512 615 3187 Email [email protected] matory abnormalities all thought to play an important role.3,6 submit your manuscript | www.dovepress.com Clinical, Cosmetic and Investigational Dermatology 2017:10 17–23 17 Dovepress © 2017 Friedmann et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms. php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work http://dx.doi.org/10.2147/CCID.S95830 you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). Friedmann et al Dovepress Nürnberger and Müller4 first proposed that topographic and disturbances in tissue oxygenation, whereas the latter alterations of cellulite skin were caused by fat herniation into is protective against fibroinflammatory and microhypoxic a weakened dermis. Although Mirrashed et al7 demonstrated, tissue responses.17 Nevertheless, biopsy examination of by magnetic resonance imaging (MRI), that cellulite grade cellulite by Rosenbaum et al11 did not show significant correlated with the percentage of hypodermic invaginations differences in regional blood flow between cellulite and into the dermis, Pierard et al8 were unable to find a correla- control sites. tion between fat protrusions and the clinical appearance of Inflammatory factors have been associated with the cellulite. Instead, they proposed that continuous and pro- pathogenesis of cellulite, with the thought that chronic gressive tension placed on vertically oriented subcutaneous inflammation may play a role in the fibrous septal develop- fibrous septae tethered to the underside of the dermis by fat ment. Significant decreases in the subcutaneous expression accumulation that alters the dermal–subcutaneous interface, of adiponectin, an adipocyte-derived hormone with anti- creating dimples and depressions.9 Bulging of partitioned inflammatory, antifibrotic, and vasodilatory functions, may subcutaneous fat lobules peripherally and superficially occurs also play a role in cellulite pathogenesis.18 Measures of as a secondary event. In fact, the morphology of subcutaneous cellular oxidative stress including serum malondialdehyde fat from cellulite compared with control skin has been shown and plasma protein carbonyls may be increased in patients to be equivalent by MRI and histopathologic examination.10,11 with cellulite.19 MRI and transmission electron micrograph studies Cellulite may also be influenced by waist-to-hip ratio, have confirmed that cellulite depressions are associated but is not a result of increased body mass index (BMI) or with a significant increase in the presence and thickness of the angle of lumbar lordosis.6,20 Idiopathic cyclic edema has underlying subcutaneous fibrous septa.12,13 Although fibrous been associated with more advanced cases of cellulite.21 The septa can be found parallel to the skin surface, tilted at 45°, combination of smoking and ACE gene polymorphism was or perpendicular to the skin surface, females with cellulite significantly associated with cellulite risk.22 have a greater percentage of perpendicular septa compared with males or females without cellulite.14 Greater tension on Clinical features and severity these fibrous septae from standing, pinching, or active muscle grading contraction (due to communication with the underlying mus- Cellulite may affect any area with subcutaneous adipose culoaponeurotic system) worsens their clinical appearance, tissue. Although most often observed in the outer thighs, pos- whereas they tend to disappear when tension is minimized terior thighs, and buttocks, the hips, periumbilical abdomen, with the patient lying down. breasts, posterior arms, and posterior neck may be affected. Alterations in the vascular and lymphatic microcir- Cellulite must always be evaluated with patients stand- culation of subcutaneous adipose tissue have also been ing in anatomic position. Pinching the affected areas with purported to play an underlying role in cellulite forma- the thumb and index finger, having the patient contract the tion. Curri15 proposed that cellulite is the result of dermal underlying muscle group, and the use of tangential hard light vascular and metabolic changes similar to those found in can all help accentuate and visualize contour irregularities chronic venous stasis.3 The combination of altered precapil- in affected areas.1 lary arteriolar sphincters increasing capillary permeability Nürnberger and Müller4 proposed the first clinical grading and glycosaminoglycan (GAG) deposition in capillary scale for cellulite, dividing the condition into three grades walls attracting water would lead to dermal edema, with with grades II and III further subclassified into mild, moder- subsequent vascular congestion, capillary network loss, ate, or severe. Grade I skin is smooth at rest, grade II skin and tissue hypoxia.13,15 Hypoxia and GAG deposition demonstrates a mattress or orange peel appearance at rest, and would, in turn, elicit neovascularization and thickening and grade III skin has grade II features and nodules intermixed sclerosis of fibrous septae. Although Lotti et al16 confirmed with raised and depressed areas at rest. the presence of extracellular GAG in the dermal ground Rossi and Vergnanini2 classified cellulite based on the substance of cellulite-affected skin, Querleux et al14 did not presence and severity of clinical and histopathologic findings, demonstrate increased water at the dermal–subcutaneous from grades I to IV. Grade I cellulite is clinically inapparent junction. ACE rs1799752 and HIF1A rs11549465 gene but may have early positive histologic changes. Grade II cellu- polymorphisms in subcutaneous tissue have also been asso- lite is clinically inapparent at rest, but dimples or depressions ciated with cellulite; the former may increase ACE activity become evident with skin pinching or muscular contraction. 18 submit your manuscript | www.dovepress.com Clinical, Cosmetic and Investigational Dermatology 2017:10 Dovepress Dovepress Cellulite Grade III and IV cellulites are clinically apparent at rest, Stimulation of cutaneous microcirculation, promotion of with the latter
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