Cellulite formation emanates from deterioration of the dermal vasculature particularly loss of the capillary networks resulting in excess fluid retained within the dermal subcutaneous tissues. This loss of capillary network is thought to be due to engorged fat cells clumping together and inhibiting venous return, thus creating a toxic environment that results in an inflammatory condition.

The fat deposition is hormonally mediated (estrogen dominance) accounting for the increased number of women affected by cellulite and the propensity for upper thigh involvement. As well, the fascia, the connective tissue comprised of collagen is progressively weakened by estrogen. The fascia ultimately loses its ability to contain the fat mass, which is normally contained in well-organized chambers separated by septa of connective tissue.

 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. Ultrasonic imaging of the skin affected by cellulite reveals a vascular inflammatory condition caused by reactive protein formed around adipose tissue in the subcutaneous hypodermis, thus the cumulative build-up of fat and protein accompanied by stiffening and deterioration of collagen causing the ‘orange peel’ appearance known as cellulite.