Although MRI has provided a sophisticated look at the histology of cellulite, the pathogenesis of this condition is still unknown. Contrary to popular belief, physical conditioning and a healthy diet do not prevent the development of cellulite. A variety of topical treatments, massage-based therapies, and surgical and laser techniques have been used to reduce
A. Bassas-Grau, et al. (1964) Edema causes cellulite in the subcutaneous connective
matrix of women
B. Querleux et al. (2002) Laxity of fibrous septae in women leads to fat herniation and
cellulite
C. Kligman et al. (1997) Inflammatory factors and vascular changes cause cellulite
*Several conflicting theories about cellulite pathogenesis.
cellulite, and most have had suboptimal clinical effects. Discovering the best treatment plan for cellulite has been the focus of many scientists and journal publications. However, finding a solution raises even more of a challenge when a consensus as the exact definition and aetiopathology of cellulite has not yet been reached. Surprisingly, scientists are still debating over three conflicting theories that relate to the ethiopathogenesis of cellulite (Table 16.1).
The first of three contradictory theories indicates that excessive hydrophilia of the intercellular matrix causes edema and fibrosclerosis. Bassas-Grau et al. noted that the subcutaneous connective matrix of women with cellulite had an excess of hyperpolymerized acid mucopolysaccharides, which thereby caused edema [11]. Although no other evidence supports the claims of Bassas-Grau, this hypothesis justified the use of topical treatments such as hyaluronidase, which had a therapeutic influence on cellulite treatment for many years.
A second theory focuses on the anatomical conformation of the female subcutaneous tissue as compared to male anatomy. This theory reflects on the works of Querleux, who through MRI confirmed the different orientation of the connective septae bands in women compared to men. According to the data, MRI rules out the possibility of edema occurring in between the adipocytes, but confirms the laxity of the fibrous septae in women, which leads to fat herniation and the lumpy appearance of cellulite [1].
Finally, a third theory attributes the cause of cellulite to inflammatory factors and vascular changes. From biopsies of cellulite, Kligman has claimed that chronic inflammatory cells, such as macrophages and lymphocytes, are diffusely concentrated in the fibrous septae. This phenomena, according to Kligman, attributes the cause of adipolysis and minor inflammation in cellulite patients to these fibrous septae [12].