Publications (2)6.34 Total impact
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ABSTRACT: The goals of this study were to develop a new intramedullary, rotation-stable locking device and evaluate it biomechanically and in vivo for maintenance of a critical size osteotomy gap in a model of conscious pseudarthrosis. In standardized osteotomized rat femora (5 mm osteotomy gap) two different rotation- and axial-stable locking devices (group pS + cS) were tested in vitro with respect to biomechanics and compared to a control group without an additional locking device (K; n = 6 for each group). For in vivo studies, 27 male Sprague Dawley rats (250-300 g) underwent a femoral defect osteotomy of critical size and were stabilized by one of the three methods (n = 9 for each group). All groups were examined radiologically postoperatively, after 14 days, and after 12 weeks. In vitro testing revealed higher compression and torsional rigidities for the two locking devices (p < 0.05) compared to the control group (compression rigidity: pS = 103.6 +/- 13.2; cS = 91.3 +/- 10.9; K = 52.8 +/- 8.4 N/mm; torsional rigidity: pS = 5.9 +/- 0.9; cS = 4.3 +/- 1.4; K = 0.4 +/- 0.1 Nmm/ degrees ). In vivo, group K and pS exhibited up to two thirds wire dislocation and reduction of the osteotomy gap, while dislocation was less frequent in the cS group. Thus, the locking device with compression of the wire showed advantages in rotational and axial stability for a critically sized defect, though the osteotomy gap could not be maintained in all cases over the 12-week period. Nevertheless, our data corroborate the necessity of an internal fixation device with sufficient axial and rotational stability.
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ABSTRACT: Substance P is involved in nociception in both the peripheral nervous system and the CNS and has been documented to play a crucial role in the complex regional pain syndrome (CRPS). So far, however, most experimental animal models are restricted to the effect of neurokinin-1 receptor blockers to inhibit substance P and do not directly evaluate its action. Thus, this study was conducted to test the hypothesis that local application of substance P causes signs and symptoms of CRPS. For this purpose rats received a continuous infusion of either substance P or saline over 24 h delivered by a mini-osmotic pump connected to an intrafemoral catheter. Animals were analyzed at either day 1 (n=6, each group) or day 4 (n=5, each group) after start of infusion. Substance P application caused a significant and long-lasting decrease in paw withdrawal thresholds upon mechanical stimulation, while animals did not present with thermal allodynia at days 1 and 4 after onset of infusion. In addition, severe s.c. edema was observed in all animals receiving substance P. In vivo fluorescence microscopy of the extensor digitorum longus muscle of the affected hind paw revealed enhanced leukocyte-endothelial cell interaction with a significant rise in the number of leukocytes both rolling along and firmly adhering to the wall of postcapillary venules, while saline-exposed animals were free of this local inflammatory response. Muscle cell apoptosis, as assessed by in vivo bisbenzimide staining, terminal deoxynucleotidyl transferase nick end labeling analysis and caspase 3-cleavage, could not be observed in either of the animals. In summary, the present study indicates that substance P is responsible for neurogenic inflammation, including local cell response, edema formation and mechanical pain, while it seems not to contribute to the generation of thermal allodynia.
University of Rostock
Rostock, Mecklenburg-Vorpommern, Germany
- Abteilung für Unfall- und Wiederherstellungschirurgie