Scar Edge Research Articles

Management of soft-tissue trauma to the face

The management of acute soft-tissue trauma can be very challenging for the facial plastic surgeon. The goals of management of facial trauma are the preservation of form and function. These goals are particularly important in facial soft-tissue trauma, where injuries can cause not only esthetic deformities but also can affect neural function, normal mastication, visual fields, and salivary outflow. This article outlines the evaluation and treatment of acute soft-tissue facial trauma. The key components include allowing for the stabilization of the patient, complete examination of the injury and face, thorough wound irrigation and debridement of necrotic tissue, preservation of all viable tissue, tension-free closure, and realignment of important facial esthetic structures. Special consideration must be given to injuries of functional structures such as the facial nerve, ductal systems or organs, and ensuring appropriated management of these structures.

Comparison of Patient Satisfaction With Incision Cosmesis After Standard and Minimally Invasive Total Hip Arthroplasty

This study evaluated patient assessments and attitudes regarding incision cosmesis following standard and minimally invasive total hip arthroplasty 1 to 3 years postoperatively. A cosmesis questionnaire designed to elicit a score evaluating scar satisfaction was mailed to patients. Although the difference in total cosmesis score between the standard and minimally invasive groups was not statistically significant, patients with a standard incision had better scores at <1 year. One significant finding was worse responses in the minimal incision patients regarding sinking and curling of scar edges.

Characteristics of I(K) and its response to quinidine in experimental healed myocardial infarction.

Mechanisms and drug treatment of serious ventricular arrhythmias in patients with healed myocardial infarction (HMI) are incompletely understood, in part because the electrophysiology and pharmacology of myocytes from noninfarcted regions of HMI hearts are not well characterized. We studied the delayed rectifier potassium current (I(K)) and quinidine responsiveness of single left ventricular subendocardial myocytes isolated from the region remote to the border zone of healed infarct myocardium (4 to 6 mm from scar edge) in cat hearts 2 months after coronary artery occlusion. Subendocardial cells isolated from corresponding regions of normal cat hearts provided controls. I(K) activation and tail currents were recorded using whole cell, voltage clamp techniques. Membrane capacitance of cells remote to HMI (187 +/- 7 pF) was significantly greater than normal (155 +/- 6 pF; P < 0.001). Action potential durations (APDs) recorded from myocytes in remote regions were prolonged (APD90 = 247 +/- 10 msec) compared to normal (214 +/- 11 msec; P < 0.05). Quinidine (1 microM) significantly prolonged APD90 in normal cells but not in remote cells. Density of I(K) (tail current) was significantly decreased in remote cells (3.1 +/- 0.3 pA/pF) compared to normal (3.9 +/- 0.3 pA/pF; P < 0.05), and voltage-dependent activation of I(K) was shifted in the positive direction. Quinidine had significantly less incremental blocking effect on I(K) already blunted by regional hypertrophy compared to its effect on normal cells in remote cells. IC50 shifted to 0.95 microM in remote cells compared with 0.50 microM in normal cells. Cells in noninfarct region remote from the scar are hypertrophied and display altered electrophysiology. Their reduced I(K) responsiveness to quinidine may explain, in part, failure of quinidine to prolong APD in such cells. Moreover, dispersion of repolarization may be decreased by the effect of quinidine on normal cells.

Regrowth of the seagrass Thalassia testudinum into propeller scars

Regrowth of turtle grass, Thalassia testudinum Banks ex Konig, into existing propeller scars and artificial cuts was studied in a mangal estuary located in Tampa Bay, Florida. Sediments from scars and cuts and adjacent grass beds were not significantly different in relation to particle size distribution and levels of calcium carbonate. Significantly lower concentrations of total organic matter and extractable ammonium but not phosphate were detected in scars. Increases in ammonium levels coincided with the expansion of T. testudinum into a propeller scar. Seagrass blade morphology and productivity did not significantly differ in short shoots growing along the edges of scars or cuts relative to those in adjacent seagrass beds. Rhizome architectural studies revealed that apical meristems were few in number (19 to 38% of rhizomes) and randomly orientated in undisturbed grass beds (31 to 53% oriented toward center). In contrast, a greater percentage of apical meristems (78 to 88%) along the edges and in scars or cuts were directed towards the center. Full regrowth required an average of 3.5 to 4.1 years in existing propeller scars and could take up to 7.6 years in artificial cuts. The lack of changes in shoot productivity and limited production of rhizome meristems in T. testudinum result in slow regrowth in propeller cuts. The management implication is that turtle grass meadows will show long-term damage from propeller scars if not protected.

The effect of steel hardness on the performance of antiwear additives

Wear tests were performed in five oil formulations using AISI-52100 balls softened down to 35 Rc. Two configurations were used: four tempered balls, and three tempered balls with a hard spindle ball. The antiwear additives gave low wear constants at all hardnesses except for the softer balls in the four-tempered-balls configuration. Indeed, in many instances moderate softening of the steel actually reduced the rate of wear. The better additives gave wear protection by the formation of films that embedded into the softer metal surfaces forming a distinctively contorted mechanical mixture of film and metal. The mixture tended to flow in a thick sheet off the sides and trailing edge of scars on the softest steel. When wearing four softened balls the mixed layer was further deformed by the formation of meshed grooves on the scar and ring ball. The glassy films formed in oils containing ZDDP on steel of intermediate hardness developed into very large pads several microns thick and up to 300 μm long that embedded into the steel. Film material formed in base oil, and the base oil with acidless tallow did not embed in the softened steel. Wear resistance in these oils also improved with moderate degrees of softening, though steel softened to below 450 VHN wore rapidly due to scuffing.All the forms of surface damage seen on the softened steel when using the better additives were judged to be undesirable for engineering purposes, even though the nominal wear rates might be acceptable.

Spatial arrangements of microfibrils in myocardial scars: Application of antibody to fibrillin

Acute myocardial infarction kills myocytes; viable and necrotic myocytes disconnect and the ends of the viable cells become anchored to collagen fibers during reparative scar tissue formation. These anchorages have not been examined in detail, although previous studies have shown that microfibrils (MFs) concentrate at the edges of scars and at the tips of normal papillary muscles. We examined the spatial arrangements of MFs at these two sites in human hearts. Light and electron microscopic observations were made on tissue samples oriented in the long axis of myocytes and stained with monoclonal antibodies to fibrillin, a glycoprotein component of human microfibrils. MFs had identical arrangements at both sites, where they formed fibrous connections between myofibers and collagen fibers. These connections were oriented in the long axis of the muscle cells. At the myocyte ends, MFs appeared to intertwine with MFs in the normal endomysium; in the main body of the connections, MFs formed compact, 200 to 500 nm thick, fibrillin-positive fibers; and at the collagen ends, MFs splayed out among collagen fibrils. These observations indicate that MFs form myofiber-collagen fiber linkages at sites where the power of myocardial contraction is being transmitted to the extracellular connective tissue framework. Formation of such linkages seems to be an important step in the successful repair of necrotic myocardial lesions.