for the treatment of patients with features of lipoatrophy as it may lead to a reduction in peripheral fat. In general, dietary modification, exercise and switching antiretrovirals that are implicated in the lipodystrophy syndrome may improve metabolic abnormalities but the impact on body fat is very small [30].

63.8.2Surgical Treatment of HIVAssociated Facial Lipoatrophy

The most common site for lipoatrophy is the face, and is often the most distressing for the patient as it identifies them as being affected by HIV. Anatomically, facial fat lies in three planes: subcutaneous fat, fat within the SMAS layer and the deep fat pads. The deep fat of the cheek constitutes the Bichat fat sack, which has three branches: temporal, buccinator and retromandibular [31]. In the literature, facial atrophy has been attributed to either atrophy of the deep facial fat pads, or atrophy of all layers of facial fat [31]. However, one recent study which evaluated the anatomy of the buccal fat pad of Bichat in HIV-related facial atrophy reported normal position and caliber of the fat pad and suggests that the cache tic appearance of the face is likely secondary to profound atrophy of the subcutaneous tissues in these areas [8].

Surgical options for HIV-associated facial lipoatrophy include: autologous fat transfer, dermis-fat graft, flaps, rhytidectomy, malar implants and soft-tissue fillers. Autologous tissue is the ideal tissue filler for physiological reasons. The potential advantages include biocompatibility, versatility, stability and natural appearance [29].

and emphasised the importance of small grafts for more predictable results [32]. This was followed by reports of free fat autographs to fill soft-tissue defects by Czerny [33], Lexer [34] and Rehn [35]. In 1911, Bruning was the first to inject autologous fat into the subcutaneous tissue for the purpose of soft-tissue augmentation [36]. In 1912, Hollander published photographs showing the results of fat infiltration into two patients with lipoatrophy of the face [37]. In 1926, Miller wrote about his experiences with infiltration of fatty tissue through cannulas [38]. Early optimism was tempered by Peer in 1950, who demonstrated histologically that fat grafts lost approximately 45% of their weight and mass 1 year or more after transplantation [39].

Interest in autologous fat transfer diminished until the advent of liposuction surgery in the 1980s which provided plastic surgeons with semiliquid fat which could be grafted with relative ease. In the 1980s, Illouz and Fournier [40, 41] developed an approach to fat transfer by syringe harvesting called ‘microlipoinjection’. Initial experimentation with this new technique yielded variable results. In the early 1990s, Ersek reported disappointing results, with fat loss ranging from 20% to 90%, which generated a widespread negative perception of the technique [42]. Since the mid-1990s, Coleman has confirmed the efficacy and permanence of grafted fat, but stresses that this is dependent on the harvesting and grafting technique adopted [43]. Indeed, ongoing variability in results has been reported depending on choice of technique, the area treated, patient factors and surgical experience. In recent years, many different techniques have evolved and a standard procedure that is adopted by all practitioners has not yet been developed.

63.9 Autologous Fat Transfer

63.9.1History of Autologous Fat Transfer

Autologous transplantation of adipose tissue is a practice that has gained increasing popularity over the past two decades. However, the concept of fat transfer is not new. The earliest recorded human free fat transfer was by Neuber in 1893, who reported using upper extremity fat to recontour soft-tissue facial defects,

63.10 Theories of Fat Graft Survival

There have been two major theories proposed for the survival of fat grafts. The ‘host cell replacement theory’ was based on the work of Neuhof and Hirshfeld in 1923. It postulated that transplanted fat undergoes complete cell death and that histiocytes would scavenge lipid material and eventually replace all the host tissue [44]. The more popular theory in recent years is the cell survival theory, which states that some of the graft adipose tissue survives after the host reaction subsides and is based on the work of Peer [45].