The 2910-nm Fiber Laser Is Safe and Effective for Improving Acne Scarring.

BACKGROUND: Acne scarring results from the inflammation associated with acne papules, which alters dermal collagen, typically producing depressed scars. Lasers have been used to remodel skin improving the texture and appearance of acne scars. Herein, we investigate a new 2910 nm, erbium-doped, fluoride glass, fiber laser for improving acne scars. This novel laser delivers up to 5000 Hz low-energy pulses, providing a unique treatment modality. METHODS: Fourteen subjects with rolling and/or boxcar acne scars were enrolled in this study. Thirteen subjects completed the final visit and received three treatments with the 2910 nm fiber laser at 6-8-week intervals. Eight subjects were Fitzpatrick type II and five were Fitzpatrick type III. Digital images were taken pre- and 1- and 3-months posttreatment and evaluated by two blinded reviewers in a randomized fashion for improvement. Subjects and the treating physician completed a Global Aesthetic Improvement Scale (GAIS) before treatment and at each visit to subjectively evaluate treatment effect. Histological analysis was performed on ex vivo lower eyelid skin samples. Side effects were evaluated by the treating physician and included erythema, edema, and pinpoint bleeding. RESULTS: Evaluation of blinded digital images revealed a mean improvement of 47.3% ± 14.2% (mean ± SEM) 3 months following the final treatment. GAIS scores demonstrated improvement as evaluated by both the subjects and the treating physician. Side effects averaged trace-to-mild erythema, edema, and pinpoint bleeding. CONCLUSION: This study shows that the 2910 nm, erbium-doped, fluoride glass, fiber laser is safe and effective for improving the appearance of acne scars.

Low-fluence treatment with a novel fractionated 2,910-nm fiber laser improves photodamage.

BACKGROUND: Facial rejuvenation by lasers that target water has been a mainstay of esthetic laser treatments for decades. Modern lasers more commonly treat a fraction of the skin surface using ablative, semi-ablative, or nonablative pulses. METHODS: Twenty subjects with visible evidence of chronic photoaging on the face were enrolled in this study. All subjects received two full-face, single-pass treatments spaced 2 months apart with the superficial mode of a 2910 nm fiber laser with an estimated penetration depth of 10 µm, 25% coverage, delivered in a 15 mm × 15 mm square microbeam pattern. A blinded comparison of pretreatment and 3-month post-treatment images was performed. Evaluation of biopsy samples for laser-tissue effects was performed on three separate subjects and biopsies were harvested 1-day post-treatment, 1-week post-treatment, and 2-weeks post-treatment. RESULTS: Blinded evaluation of digital images revealed an average improvement score of 25.1 ± 14.5 (mean ± SEM) or 25.1%, using an 11-point scale evaluating overall improvement in photoaging (p < 0.001). Post-treatment effects were limited to mild-to-moderate erythema and edema, and the pain was rated a 1.9 out of a maximum of 10. Histology demonstrated superficial changes in the stratum corneum and epidermis with dermal inflammation present at 1-day post-treatment and 1-week post-treatment, with a return to baseline at 2 weeks. CONCLUSIONS: The 2910 nm fiber laser is safe and effective for improving mild photodamage, with minimal discomfort and downtime. Dermal inflammation results from very superficial epidermal injury and may contribute to clinical improvement.

Effects of herpes simplex virus on structure and function of nectin-1/HveC.

Herpes simplex virus (HSV) entry requires the interaction between the envelope glycoprotein D (gD) and a cellular receptor such as nectin-1 (also named herpesvirus entry mediator C [HveC]) or HveA/HVEM. Nectin-1 is a cell adhesion molecule found at adherens junctions associated with the cytoplasmic actin-binding protein afadin. Nectin-1 can act as its own ligand in a homotypic interaction to bridge cells together. We used a cell aggregation assay to map an adhesive functional site on nectin-1 and identify the effects of gD binding and HSV early infection on nectin-1 function. Soluble forms of nectin-1 and anti-nectin-1 monoclonal antibodies were used to map a functional adhesive site within the first immunoglobulin-like domain (V domain) of nectin-1. This domain also contains the gD-binding site, which appeared to overlap the adhesive site. Thus, soluble forms of gD were able to prevent nectin-1-mediated cell aggregation and to disrupt cell clumps in an affinity-dependent manner. HSV also prevented nectin-1-mediated cell aggregation by occupying the receptor. Early in infection, nectin-1 was not downregulated from the cell surface. Rather, detection of nectin-1 changed gradually over a 30-min period of infection, as reflected by a decrease in the CK41 epitope and an increase in the CK35 epitope. The level of detection of virion gD on the cell surface increased within 5 min of infection in a receptor-dependent manner. These observations suggest that cell surface nectin-1 and gD may undergo conformational changes during HSV entry as part of an evolving interaction between the viral envelope and the cell plasma membrane.