Subcutaneous fat infiltration into the dermal layer induces wrinkle formation.

BACKGROUND: Wrinkles appear with aging, producing an aged impression, but the mechanism of wrinkle formation has not yet been fully elucidated. We recently reported that subcutaneous fat infiltrates into the dermal layer with aging and impairs skin elasticity, but the contribution of this process to wrinkle formation is still unclear. PURPOSE: We aimed to clarify the contribution of dermal fat infiltration to wrinkle formation by analyzing the relationship between them in the forehead of female volunteers. METHODS: We measured the severity of fat infiltration in the forehead of 29 middle-aged female volunteers by means of ultrasonography. Fixed wrinkles present when the eyes were closed and wrinkles transiently formed when the eyes were open were evaluated using a photograph-based 6-grade evaluation system for each type of wrinkle. RESULTS: Fat infiltration at the forehead area was observed similarly to that in the cheek area as we reported previously. We found that opening the eyes induced the formation of stable transient wrinkles, the grade of which was significantly related to fat infiltration severity. Furthermore, fat infiltration was also significantly related to the severity of fixed wrinkles. Moreover, the severity of transient wrinkles was significantly related to that of fixed wrinkles. CONCLUSIONS: Our results suggest that fat infiltration into the dermal layer enhances transient wrinkle formation during facial expression by impairing the ability of the skin to resist deformation, thereby promoting fixed wrinkle formation. Therefore, fat infiltration is a critical cause of wrinkle formation.

Fat infiltration into dermal layer induces aged facial appearance by decreasing dermal elasticity.

BACKGROUND: Facial morphology changes with aging, producing an aged appearance, but the mechanisms involved are not fully established. We recently showed that subcutaneous fat infiltrates into the dermal layer with aging, but it is not yet clear whether and how this drastic change of the dermal layer influences facial appearance. PURPOSE: We aimed to establish the role of fat infiltration in producing an aged facial appearance and to clarify the mechanism involved. METHODS: We analyzed the severity of fat infiltration in cheek skin of 30 middle-aged female volunteers by means of ultrasonography. Severity of the nasolabial fold, an established age-related morphology, was evaluated based on our photographic grading criteria as a measure of aged appearance. Skin elasticity was measured with a Cutometer. RESULTS: Fat infiltration to the dermal layer was detected at the cheek skin noninvasively by means of ultrasonography. Fat infiltration severity, measured as the minimum depth of the fat inside the dermal layer from the skin surface, was positively correlated with the magnitude of the nasolabial fold. Further, fat infiltration severity was significantly negatively correlated with dermal elasticity. CONCLUSIONS: Our results suggest that fat infiltration into the dermal layer is a critical factor inducing aged appearance of the face. The infiltrated fat decreases the dermal elasticity, which exacerbates nasolabial folds, namely producing an aged facial appearance.

Increment of subcutaneous adipose tissue is associated with decrease of elastic fibres in the dermal layer.

Obesity is a significant risk factor for various skin disorders, including pressure ulcer and delayed wound healing. We previously showed that increment of subcutaneous adipose tissue contributes to poor skin condition by decreasing dermal elasticity. Here, we examined the mechanism involved. Histologic observation of abdominal skin from middle-aged females with a wide range of body mass index (BMI), an indicator of subcutaneous fat mass, showed that dermal elastic fibre abundance was significantly decreased with increment of BMI. Concomitantly, adipocytes were significantly enlarged. Adipocyte enlargement was significantly negatively correlated with dermal elastic fibre abundance. We hypothesized that enlarged adipocytes negatively influence dermal elastic fibres, so we investigated elastic fibre-degrading factors in in vitro-cultured enlarged adipocytes. MMP9 gene expression and secretion were significantly increased; further, these changes were blocked by extracellular signal-regulated kinase (ERK) inhibitor. Nuclear translocation (activation) of AP-1, a downstream ERK signalling molecule, was also observed in enlarged adipocytes. MMP9 abundance was significantly increased in skin of subjects with high BMI and enlarged adipocytes. These results suggest that increment of subcutaneous adipose tissue leads to adipocyte enlargement together with increased degradation of dermal elastic fibres, mediated at least in part by an ERK signalling-mediated increase of MMP9 in enlarged adipocytes.