The platelet-rich plasma (PRP) has been studied in bone-related applications for accelerating healing, and the proliferation and regeneration of tissue. Now the dermatological indications increase rapidly in recent years. We have reviewed clinical trials, comparative trials, and meta-analysis of PRP on dermatology through key words and reorganized them into facial rejuvenation, hair, scar, vitiligo, and synergistic effect with fractional CO , with a conclusion that PRP has significant improvements in dermatology. But the lack of RCTs and the limit of samples cannot provide sufficient enough evidence for general clinical applications. More RCTs are needed for the increasing demand of new dermatologic therapeutics, and we need adequate samples urgently to make the results more persuasive.

Ultraviolet B (UVB) is one of the most common exogenous factors in skin aging, especially photoaging. Once a large amount of UVB accumulates within a short period of time, skin tissue can become inflamed. It has also been found in clinics that platelet-rich plasma (PRP) can promote wound repair; therefore, the aim of this study was to identify the mechanism by which PRP repairs UVB-induced skin photodamage. We used PRP of Sprague-Dawley rats with the two-spin technique in the established acute UVB radiation photodamage model and harvested the corresponding skin after 1, 7, and 28 d. Hematoxylin and eosin staining was used to observe tissue inflammation. We found that PRP reduces inflammation in the early stages of UVB-induced acute skin damage, and then promotes the proliferation of collagen in the middle and late stages. Moreover, PRP can stimulate Act A and M1 polarization in the early stage, while inhibiting activin A (Act A) and inducing M2 polarization in the middle and late stages. In conclusion, this study demonstrates that PRP plays an important regulatory role in helping reduce UVB-induced acute skin tissue inflammation by adjusting macrophage polarization, which alleviates skin inflammation and stimulates collagen regeneration.

Costello syndrome (CS) is a rare autosomal dominant genetic disease, which was first described by Costello in 1997 based on its distinctive phenotype. The characteristic symptoms of CS are as follows: growth delay, intellectual disability, dermatologic anomalies, cardiac problems, musculoskeletal abnormalities, special facial features, and a predisposition to developing neoplasia (Rauen, 2007). In most cases, Costello syndrome is caused by specific heterozygous, de novo variants in HRAS gene (