INTRODUCTION
Aesthetic treatments are becoming increasingly popular among patients, especially nonsurgical procedures.1 According to statistics from the American Society of Facial Plastic Surgery (ASAPS), there was a 37.6% increase in the number of nonsurgical treatments from 2012 to 2017.2 Rejuvenation of non- facial areas is becoming a frequent complaint in patients who recognize the disparity and stigma that arise between their treated face and their non-treated body areas.
The biochemical properties of the skin are determined by the epidermis, dermal collagen and elastin network and subdermal composition.3,4 The capacity to synthesize collagen is lower in sun exposed and aged skin than in healthy, young skin. Fibroblasts in severely damaged skin (either photoaged, naturally aged, or both) experience a loss of mechanical tension as a result of decreased interaction with intact collagen, which in turn leads to a diminished production of skin macromolecules.5,6 The body mass index (BMI) of the patient, which may be used as an indicator for tissue composition, has a negative correlation with skin firmness and thickness, and a positive correlation with energy absorption.4 When patients present with body sculpting concerns, most often there is both a component of fat excess and skin laxity, with a decrease in neocollagenesis at fibrous septae and fascial planes level that accounts for changes that bother them.1 It is important to perform a correct diagnosis of the involved components in order to select the best candidates for PLLA treatments.
As we age, the cellular turnover rate declines, and skin structure begins to deteriorate. Age-related skin changes include:
1) Increase in the disorderly arrangement of the collagen fiber network7
2) Decrease in the quantity of fibroblasts8
3) Decline in collagen production by fibroblasts8
4) Increase in matrix metalloproteinases levels, the primary enzymes responsible for degradation of collagen fibers8
5) Decreased metabolic activity of the skin9
6) Massive elastosis or deposition of abnormal elastin fibers, exaggerated microvasculature, and collagen degeneration9
The biochemical properties of the skin are determined by the epidermis, dermal collagen and elastin network and subdermal composition.3,4 The capacity to synthesize collagen is lower in sun exposed and aged skin than in healthy, young skin. Fibroblasts in severely damaged skin (either photoaged, naturally aged, or both) experience a loss of mechanical tension as a result of decreased interaction with intact collagen, which in turn leads to a diminished production of skin macromolecules.5,6 The body mass index (BMI) of the patient, which may be used as an indicator for tissue composition, has a negative correlation with skin firmness and thickness, and a positive correlation with energy absorption.4 When patients present with body sculpting concerns, most often there is both a component of fat excess and skin laxity, with a decrease in neocollagenesis at fibrous septae and fascial planes level that accounts for changes that bother them.1 It is important to perform a correct diagnosis of the involved components in order to select the best candidates for PLLA treatments.
As we age, the cellular turnover rate declines, and skin structure begins to deteriorate. Age-related skin changes include:
1) Increase in the disorderly arrangement of the collagen fiber network7
2) Decrease in the quantity of fibroblasts8
3) Decline in collagen production by fibroblasts8
4) Increase in matrix metalloproteinases levels, the primary enzymes responsible for degradation of collagen fibers8
5) Decreased metabolic activity of the skin9
6) Massive elastosis or deposition of abnormal elastin fibers, exaggerated microvasculature, and collagen degeneration9
