Edematous fibrosclerotic panniculopathy (Cellulite)

Edematous fibrosclerotic panniculopathy (EFP), commonly known as cellulite, has been defined as a local metabolic disorder of subcutaneous tissues that results in a contour abnormality of the skin.1 The condition manifests as dimpled skin, particularly in the gluteal-femoral region.2,3 EFP is caused by herniation of subcutaneous fat lobules through the dermohypodermal junction and/or shortening of the collagen septa that cross the hypodermal layer and connects the dermis to the underlying fascia. This creates an uneven surface with dimpling.1,2 EFP is a medical condition resulting in a potentially cosmetically unacceptable alteration of the skin, and affects an estimated 85% to 98% of postpubertal women.1,3

The pathophysiology of EFP is not completely understood, but there are 3 main theories: edema resulting from excessive hydrophilia of the intercellular matrix, alteration of the regional microcirculation, and different anatomical conformation of collagenous subcutaneous tissues in women versus men.4

It is known that EFP is different from generalized obesity. In generalized obesity, adipocytes undergo hypertrophy and hyperplasia that are not limited to the pelvis, thighs, and abdomen.1 In areas of EFP, characteristic large, metabolically stable adipocytes have physiologic and biochemical properties that differ from adipose tissue located elsewhere.

Subcutaneous fat lobes are separated from one another by thin, usually rigid strands of collagenous connective tissues, which cross the fatty layers and connect the dermis to the underlying fascia. These septa stabilize the subcutis and divide the fat. In EFP, shortening of the collagen septa due to fibrosis provokes retraction at the insertion points of the trabeculae, causing the depressions that characterize EFP.2 There are a higher percentage of thinner, perpendicular hypodermal septa in women with EFP than in men.1 Weight gain makes EFP more noticeable, but it may be present even in thin subjects. Genetics may also play a role since EFP tends to run in families.


  1. Khan MH, Victor F, Rao B, Sadick NS. Treatment of cellulite: Part I. Pathophysiology. J Am Acad Dermatol 2010;62(3):361-370.
  2. Hexsel D, de Oliveira Dal’Forno T, Mazzuco R. Definition, clinical aspects, classifications, and diagnostic techniques. In: Goldman MP, Hexsel D, eds. Cellulite: Pathophysiology and Treatment. 2nd ed. New York, NY: Informa Healthcare; 2010:13-21.
  3. Rawlings AV. Cellulite and its treatment. Int J Cosmetic Sci. 2006;28(3):175-190.
  4. Terranova F, Berardesca E, Maibach H. Cellulite: nature and aetiopathogenesis. Int J Cosmetic Sci. 2006;28(3):157-167.

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