Acne Scars

J Mol Cell Cardiol. 2009 Jul 22; Dobaczewski M, Gonzalez-Quesada C, Frangogiannis NGThe dynamic alterations in the cardiac extracellular matrix following myocardial infarction not only determine the mechanical properties of the infarcted heart, but also directly modulate the inflammatory and reparative response. During the inflammatory phase of healing, rapid activation of matrix metalloproteinases (MMP) causes degradation of the cardiac extracellular matrix. Matrix fragments exert potent pro-inflammatory actions, while MMPs process cytokines and chemokines altering their biological activity. In addition, vascular hyperpermeability results in extravasation of fibronectin and fibrinogen leading to formation of a plasma-derived provisional matrix that serves as a scaffold for leukocyte infiltration. Clearance of the infarct from dead cells and matrix debris is essential for resolution of inflammation and marks the transition to the proliferative phase. The fibrin-based provisional matrix is lysed and cellular fibronectin is secreted. ED-A fibronectin, mechanical tension and Transforming Growth Factor (TGF)-beta are essential for modulation of fibroblasts into myofibroblasts, the main collagen-secreting cells in the wound. The matricellular proteins thrombospondin-1 and -2, osteopontin, tenascin-C, periostin, and secreted protein acidic and rich in cysteine (SPARC) are induced in the infarct regulating cellular interactions and promoting matrix organization. As the infarct matures, matrix cross-linking results in formation of a dense collagen-based scar. At this stage, shielding of fibroblasts from external mechanical tension by the mature matrix network may promote deactivation and cellular quiescence. The components of the extracellular matrix do not passively follow the pathologic alterations of the infarcted heart but critically modulate inflammatory and reparative pathways by transducing signals that affect cell survival, phenotype and gene expression.

Am J Dermatopathol. 2009 Jul 23; Wiedemeyer K, Kutzner H, Abraham JL, Thakral C, Carlson JA, Tran TA, Hausser I, Hartschuh WGadolinium (Gd) is associated with nephrogenic systemic fibrosis (NSF), a severe disorder mimicking scleroderma with involvement of the skin, lungs, heart, liver, and muscles. There is strong evidence that specific Gd-containing contrast agents (GCCAs) used in magnetic resonance imaging can cause NSF when administered to patients with chronic kidney disease. We present the 8-year history of cutaneous NSF with osseous metaplasia that occurred in a 56-year-old man with dialysis-dependent renal failure who was exposed to GCCA [gadopentate dimeglumine (Magnevist; Bayer Schering Pharma AG, Pittsburgh, PA)]. Three months after exposure to GCCA, he developed pruritic, pigmented patches that slowly coalesced and darkened over 8 years. Although not recognized at onset, skin biopsy showed typical histology of NSF affecting the entire dermis: CD34/procollagen I spindle cells associated with fibrosis. Biopsy performed 6 years later showed superficial scar-like fibrosis that was CD34/procollagen I and had numerous elastocollagenous balls (refractile elastic fibers surrounded by coarse collagen). Biopsy 7 years later showed the superimposition of osseous metaplasia on elastocollagenous balls. Both of these later biopsies had typical NSF histology affecting the deep dermis and subcutis. Over time, there was progressive diminishment of CD34 and procollagen I+ cells and an increase in FXIIIa+ and CD68 cells. Scanning electron microscopy and energy-dispersive x-ray spectroscopy showed Gd deposits in all areas of typical NSF histology but not in the regions of scar-like fibrosis, elastocollagenous balls, or osseous metaplasia. We suspect that the later changes may represent a late, involuting stage of NSF.

J Craniofac Surg. 2009 Jul; 20(4): 1280-2Hwang KThe aim of this study is to determine the safety and complication of subciliary approach through the retrospective review of our experiences. From 2005 through 2008, the subciliary skin-muscle flap methods were used in 30 patients undergoing medial orbital wall reconstruction. Preoperative and postoperative ophthalmic findings including diplopia, Hertel exophthalmometry, and occurrence of complications were checked. Resorbable polylactic acid sheet or porous polyethylene sheet was trimmed and molded in L shape, vertical portion to cover the medial wall defect and horizontal portion for stability in orbital floor.In the follow-up of diplopia, half of the patients (3 cases) presenting with diplopia improved during the first month of follow-up, and all of them improved by 6 month. For hypesthesia, all patients improved by 3 months. Enophthalmos of 1 patient improved after operation and did not recur. No patients complained of visible scar 6 months postoperatively, and no ectropion was observed.We think that medial orbital wall could be reconstructed safely through skin-muscle flap subciliary approach without resulting in ectropion or lacrimal canaliculus injury.

Ophthalmic Res. 2009 Jul 23; 42(3): 152-154Quijano C, Querques G, Massamba N, Soubrane G, Souied EHAim: To describe a patient with type 3 choroidal neovascularization (CNV) associated with fundus flavimaculatus (FFM), who underwent treatment with intravitreal ranibizumab. Methods: A 78-year-old woman diagnosed with FFM presented at our department complaining of decreased vision and metamorphopsia in her left eye. Upon a complete ophthalmologic examination, including best corrected visual acuity (BCVA), fundus autofluorescence, fluorescein angiography (FA), indocyanine green angiography (ICGA), and spectral domain optical coherence tomography (SD-OCT), the patient was diagnosed with type 3 CNV associated with FFM, and was submitted to intravitreal ranibizumab injections at monthly intervals. Results: Six months after 3 monthly injections of ranibizumab, the patient's BCVA improved from 20/64 to 20/32. FA and ICGA revealed a type 3 CNV closure, and the SD-OCT scan showed a fibrous scar replacing the type 3 CNV, with resolution of serous retinal detachment. Conclusion: This case represents the first demonstration of type 3 CNV associated with FFM. Based on our findings, intravitreal ranibizumab may be considered as a therapeutic option for this rare association.