The aim of the study was to investigate the long-term effects of postoperative immobilization as opposed to mobilization on the biomechanical attributes of healing Achilles tendons in a new experimental mouse model. Postoperative mobilization resulted in a continuous and significantly more rapid restoration of load to failure in comparison to the immobilization group. Tendon deflection was decreased by postoperative mobilization, whereas under immobilization it paradoxically increased still further in the later course. After 112 days the tendons of the mobilization group had regained their original tendon stiffness, whereas the tendons after immobilization reached only about half the values seen in the control tendons. Histologically, postoperative mobilization led to increased immigration of inflammatory cells in the early phase. In the late phase, as compared to immobilization, tendon structure was more mature, with fibre bundles arranged in parallel and interposed tendocytes.Tensile loading of the healing tendon by postoperative mobilization leads to fundamental changes in the biological process of tendon healing resulting in accelerated restoration of load to failure and reduced tendon deflection.

The extent of callus formation about a bone fracture depends on the rigidity of fracture fixation. The mechanism that converts the mechanical stimulus into the biologic response is unknown. On the basis of existing literature, an attempt has been made to define a model that explains this mechanobiologic transduction. Once integrity of the bone has been disrupted, a sequence of biochemical and cellular events commences that induces inflammatory reactions. Messengers (e.g., metabolites of the clotting or complement system, eicosanoids, or growth factors) are released or activated. They control the migration, proliferation, and protein synthesis of cells that are essential for angiogenesis and connective tissue formation. The key component in this inflammatory sequence seems to be the macrophage. Growth factors (e.g., released by macrophages) stimulate endothelial cells to form capillaries and mesenchymal cells to synthesize their matrix. In mechanically neutral areas, the fracture cavity is revascularized and osteoblasts proliferate and form bone. In mechanically instable fracture areas, spreading capillaries are disrupted by shear forces. In these areas, therefore, the milieu becomes hypoxic again. This milieu seems to support the differentiation of chondrocytes that stabilize the fracture by cartilage formation. If the strength of repair tissue is surpassed, the disrupture of the repair tissue triggers the mechanisms of inflammation again and additional cells immigrate and proliferate. Their protein synthesis increases repair callus. The increase of callus formation, however, stops when the tissue is capable of resisting motion. Links to the callus formation in osteitis are shown.

No abstract

Mechanical conditions at the fracture line determine the mode of fracture healing (osteonal versus non-osteonal bone union). The aim of this study was to investigate the influence of differing degrees of fracture stability on the time course of chondrogenesis, enchondral ossification and immigration of macrophages into the fracture callus.Using a fracture model of the rat's tibia, histological (Azan staining), immunohistological (antibodies directed against the macrophage-specific surface antigen ED2), and molecular biological techniques (expression of the mRNA of the cartilage-specific collagen IX, osteocalcin -a marker for mature osteoblasts -and the macrophage-specific macrosialin) were employed.In terms of histology and molecular biology (collagen IX mRNA expression) chondrogenesis in the fracture gap continued for longer in less stable fractures. In more stable fractures bone formation -identified by osteocalcin mRNA expression -increased from day 12 onwards. The expression of the macrophage-specific surface antigen ED2 and the mRNA of macrosialin was more pronounced but of shorter duration in the more stable fractures.This study shows that differing degrees of fracture stability not only influence the interplay between osteogenesis and chondrogenesis but also alter the kinetics of macrophage immigration into the fracture callus. These findings could aid in better understanding the cytobiologic mechanisms of callus formation and may suggest that macrophages are an important factor not only in soft tissue healing but also in bone healing.

We report on 17 patients with GAVE-syndrome (gastric antral vascular ectasia) treated by means of endoscopic argon plasma coagulation (APC). 16 of 17 patients presented with iron deficiency anemia; transfusion-dependent anemia was noted in 11 patients (65%). Resolution of the gastric angiectasia could be achieved in all patients by endoscopic APC after 1-4 treatment sessions. Endoscopic follow-up revealed recurrence of GAVE in 5 patients (requiring further treatment sessions). Mean pretreatment hemoglobin level of 78 g/l improved to 115 g/l after treatment. Only one patient needed post-treatment transfusions; she had refused further endoscopy. The mean follow-up was 30.4 months (range 1-65). In one case circumferential scarring of the antrum led to asymptomatic stenosis 6 months after APC; at the same time early recurrence of extensive angiectasia occurred. Billroth I resection was performed. No other complications were observed. Our results show that argon plasma coagulation is an effective and safe treatment for gastrointestinal blood loss due to GAVE syndrome (watermelon stomach). Control endoscopies are indicated in order to recognize and treat recurrence of angiectasia on time.