Multipass Vector (Mpave) Technique with Nonablative Radiofrequency to Treat Facial and Neck Laxity

Background. Redundant facial and neck skin is a major feature of aging and historically has been corrected surgically. Recently, monopolar radiofrequency application has been introduced for nonablative tissue tightening of skin by volumetric heating of the deep dermis. It has been able to improve neck and cheek laxity and periorbital rhytides and to elevate eyebrows. However, questions remain as to the ideal parameters needed to optimize the use of radiofrequency.
Objective. To determine the safety and report on the efficacy of a radiofrequency application that involves a multipass vector (mpave) technique to target facial and neck skin laxity.
Methods. Twenty-five patients (skin types I to V) with mild to severe facial and neck laxity received one treatment session with monopolar radiofrequency. Treatment parameters, adverse events, and digital photographs were recorded. All patients were treated with a multipass vector technique consisting of four to five passes targeted over areas of skin that would most improve facial laxity. The multipass vector (mpave) treatment approach is described. Energy levels ranged from 62 to 91 J/cm2 per pulse.
Results. All patients experienced some immediate erythema and edema, which had completely resolved in most patients within 48 hours. No scarring or dyspigmentation was noted on follow-up at 6 and 12 weeks. Photographic analysis of pre- and post-treatment digital images revealed cosmetic improvement in facial and neck laxity in 96% of patients. The majority of patients demonstrated a moderate or better improvement. Stacked pulses in the submental region were shown to reduce fat.
Conclusions. The direct application of monopolar radiofrequency to facial and neck skin using a multipass vector (mpave) treatment approach was safely tolerated in patients of all skin types. Patient satisfaction correlated well with photographic analysis, and the technique was shown to be efficacious for most patients.     

A simple in vitro model for investigating epithelial/mesenchymal interactions: keratinocyte inhibition of fibroblast proliferation and fibronectin synthesis

Hypertrophic scarring and graft contracture are major causes of morbidity after burn injuries. It is well established that application of a split-thickness skin graft reduces scarring and contraction, and cultured epithelial autografts have a similar effect. To investigate the influence of keratinocytes on fibroblast proliferation and fibronectin synthesis, we used an in vitro separated co-culture model in which epithelial sheets were cultured above fibroblast monolayers without physical contact. We also investigated the response of fibroblasts to keratinocyte-conditioned medium (KCM) obtained from confluent and subconfluent keratinocyte monolayers. Both cultured epithelial sheets, composed of adherent fully confluent keratinocytes, and their conditioned medium, reduced fibroblast proliferation. However, KCM from subconfluent keratinocytes stimulated fibroblast proliferation at low concentrations while inhibiting it at higher concentrations, indicating that keratinocytes can produce both mitogenic and growth-inhibiting factors for fibroblasts. KCM, but not epithelial sheet co-culture, also inhibited fibroblast fibronectin synthesis. This indicates regulation of fibroblast phenotype by soluble factors released by the keratinocyte and also suggests that there is a dialogue between keratinocytes and fibroblasts with respect to fibronectin production. We conclude that this separated co-culture model is a simple way to study epithelial/mesenchymal communication particularly with respect to the role of the fibroblast in wound healing.     

Development of an in vitro burn wound model

Healing of a deeper burn wound is a complex process that often leads to scar formation. Skin wound model systems are important for the development of treatments preventing scarring. The aim of this study is to develop a standardized in vitro burn wound model that resembles the in vivo situation. A burn wound (10 × 2 mm) was made in ex vivo skin and the skin samples were cultured at the air–liquid interface for 7, 14, and 21 days. Cells in the skin biopsies maintained their viability during the 21-day culture period. During culture, reepithelialization of the wound took place from the surrounding tissue and fibroblasts migrated into the wound area. Cells of the epithelial tongue and fibroblasts near the wound margin were proliferating. During culture, skin-derived antileukoproteinase and keratin 17 were expressed only in the epithelial tongue. Both collagen type IV and laminin were present underneath the newly formed epidermis, indicating that the basement membrane was restored. These results show that the burn wound model has many similarities to in vivo wound healing. This burn wound model may be useful to study different aspects of wound healing and testing pharmaceuticals and cosmetics on, e.g., migration and reepithelialization.     

Comparison of a Chronotherapeutically Administered β Blocker vs. a Traditionally Administered β Blocker in Patients With Hypertension

Increasing systolic blood pressure and heart rate during the early morning results in increased myocardial oxygen demand. The use of β blockers during this period may decrease cardiac workload, particularly in β-blocker sensitive patients. The impact of a new chronotherapeutic β blocker was assessed in 44 hypertensive patients. Patients were randomized to delayed-release propranolol (INP) dosed at 10 p.m. or to traditionally dosed propranolol (ILA) dosed at 8 a.m. for 4 weeks, following which they were switched to the alternative formulation for 4 weeks. Thirty-four-hour ambulatory blood pressure monitoring and pharmacokinetic measurements were obtained. INP and ILA resulted in significant reductions in mean 24-hour blood pressure (−9.01-6.9 mm Hg and −10.41-7.7 mm Hg, respectively). The top 25% of responders to highdose propranolol (sensitive patients) were compared on each formulation. Mean trough reductions were −8.0/-6.7 mm Hg and −7.61-5.8 mm Hg, respectively. Mean blood pressure reductions in the β-blocker sensitive patients (n=11) between 6 a.m. and noon were −15.2/-11.9 mm Hg on INP and -8.0/-4.6 mm Hg on ILA. Heart rate reduction was −14.1 bpm and double product reduction was −3319 in the INP patients between 6 a.m. and 12 noon compared with −10.5 and −2209 in the ILA patients. This study suggests that INP and ILA are effective once-a-day β blockers, but the use of delayed-release propanolol results in a greater reduction in double product between 6 a.m. and noon in β-blocker sensitive patients than does traditionally dosed propranolol.     

Growth hormone effects on hypertrophic scar formation: a randomized controlled trial of 62 burned children

The hypercatabolism after massive pediatric burns has been effectively treated with recombinant human growth hormone, an anabolic agent that stimulates protein synthesis and abrogates growth arrest. While experimental studies have shown increased potential for fibrosis induced by growth hormone therapy, adverse effects on human scars have not been investigated. Our aim was to evaluate hypertrophic scar formation in 62 patients randomized to receive injections of 0.05 mg/kg/day of recombinant human growth hormone or placebo, from discharge until 1 year after burn. Scar scales were used to evaluate scar-severity at discharge, 6, 9, 12, and 18-24 months after burn, by three observers blinded to treatment. Computer-assisted planimetry allowed quantification of percentage of hypertrophic scar formation. Types I and III collagens were localized and quantified in scars and normal skin of patients from both groups, using immunohistochemistry with confocal laser microscopy analysis. Insulin-like growth factor-1 blood levels helped assess compliance. Statistical analysis showed that scar hypertrophy significantly increased from 6 to 12 months after injury in both groups, while decreasing at 18-24 months postburn. Types I and III collagens were statistically increased in the reticular layer of scars from both groups when compared to paired normal skin. Insulin-like growth factor-1 was significantly increased in the recombinant human growth factor-treated group. No differences were seen when recombinant human growth factor and control groups were compared using the scar scales, planimetry, or immunohistochemistry. We concluded that recombinant human growth hormone therapy did not adversely affect scar formation and should not contraindicate the administration of recombinant human growth hormone as a therapeutic approach to severely burned children.