Aims: The roentgenologic morphology of symptomatic calcified deposits of the rotator cuff can be classified according Gärtner (1993, Z Orthop Ihre Grenzgebiete 131: 461–469). This classification influences therapeutic procedures and prognosis of clinical outcome in these patients. In the present study intraoberserver-reproducibility and interobserver-reliability of Gärtner’s classification were tested. Methods: Plane radiographs of 100 patients with calcifications of the supraspinatus tendon were classified according the criteria of Gärtner by six independent observers twice within four months. Intrao-berserver-reproducibility and interobserver-reliability were calculated by means of Cohen’s-kappa-index. Results: Kappa-values of intraoberserver-reproducibility had a mean of 0.4208 (SD 0.1299), kappavalues of interobserver-reliability were 0.490 for the first and 0.474 for the second classification. Conclusions: Determination of intraoberserverreproducibility gave insufficient to satisfactory results, interobserver-reliability was sufficient. The clinical use of Gärtner’s classification to plan therapeutic procedures or to determine clinical prognosis in patients with calcifying tendinitis can be recommended only with limitations.

Aims: Little is known about effects of extracorporeal shock wave application (ESWA) on normal bone physiology. Therefore, we investigated ESWA effects on intact distal rabbit femura as an in vivo animal model. Methods: Animals received 1,500 SW pulses each of different energy ßux densities (EFD) on either left or right femur or remained untreated. ESWA effects were investigated by bone scintigraphy, MRI and histopathological examination. Results: Ten days after ESWA, local blood ßow and bone metabolism were decreased (0.5 mJ/mm2 and 0.9 mJ/mm2 EFD), but were increased 28 days after ESWA (0.9 mJ/mm2). ESWA with 0.9 mJ/mm2 EFD (but not with 0.5 mJ/mm2 ) resulted in MRI signs of soft-tissue-edema, epiperiosteal ßuid and bone marrow edema one day after ESWA, as well as in hemosiderin deposits found epiperiosteally and within the marrow cavity ten days after ESWA. Conclusions: ESWA with both 0.5 mJ/mm2 and 0.9 mJ/mm2 EFD had effects on normal bone physiology in the distal rabbit femur, with considerable damaging side effects of ESWA with 0.9 mJ/mm2 EFD on periosteal soft tissue and tissue within the bone marrow

Nitric oxide (NO) production by the inducible NO synthase (iNOS) and enhanced emigration of leukocytes into synovial tissue are suggested to play a crucial role in mediating chronic joint inflammation such as rheumatoid arthritis. The effects of iNOS inhibition in experimental arthritis are dicussed controversally. The aim of our study was to analyze the synovial microcirculation and leukocyte endothelial cell interactions in iNOS-deficient mice with antigen-induced arthritis (AiA) in vivo. 14 homocygote iNOS-deficient (iNOS KO C57BL6/J x 129SvEv; Merck & Co., Rahway, NJ, USA) and 14 iNOS-positive (C57BL6/J x 129SvEv) mice were used for our study. The patella tendon was resected, which allows for visualization of the intraarticular synovial tissue of the knee joint using intravital fluorescence microscopy. Animals were allocated into four groups (iNOS +/+, iNOS +/+ with AiA, iNOS −/− and iNOS −/− with AiA) (n=7 each group). On day 8 after arthritis induction, functional capillary density (FCD), fraction of rolling leukocytes, and the number of adherent leukocytes were quantitatively analyzed in synovial postcapillary venules. Histologic sections were performed to assess leukocyte infiltration of the synovium.

FCD or leukocyte-endothelial cell interaction were not altered in healthy iNOS-deficient mice in comparison to iNOS +/+ animals. However, in iNOS-deficient animals with AiA there was a significant increase in the fraction of rolling (0,510,05) and in the number of adherent leukocytes (729126 mm-2) in comparison to wild type mice with AiA (0,330,07 and 565110 mm-2) (MWSEM, p < 0,05). Histologic sections revealed increased leukocyte infiltration in iNOS-deficient animals with AiA compared to iNOS +/+ arthritic animals.

In our study, there was an enhanced leukocyte accumulation and extravasation in iNOS-deficient mice with antigen-induced arthritis in comparison to iNOS-positive animals with arthritis. Thus, the induction of iNOS appears as critical protective response to AiA possibly by reducing leukocyte adhesion and infiltration.

Edema and infection represent serious complications of blunt extremity trauma. It is important to differentiate between pathophysiological changes within tissues proximal and within distal to the site of trauma. The aim was to investigate the effects of soft tissue trauma on the microcirculation of the mouse lower limb. Endothelial leakage and leukocyte accumulation proximal and distal to the site of trauma were studied using intravital fluorescence microscopy.

Low-energy trauma to the lower limb was defined in previous experiments as a trauma transferring 50% of the energy required to produce tibial fracture. The trauma was inflicted under general anesthesia by an accelerator, hitting the mid-section of the calf in a perpendicular direction. 5, 90, and 180 minutes after trauma, the following microcirculatory parameters were measured: diameter of arterioles, venules, functional capillary density (FCD), extravasation of FITC-dextrane, and leukocyte-endothelial cell-interactions. Two groups (control and trauma) were studied proximal to, distal to and at the site of trauma. Skin, subcutaneous tissue and muscle were investigated individually in the trauma and the control groups (each group n=7).

At the site of trauma, distinct extravasation and edema formation in all tissues was observed. In subcutaneous and muscle tissue, microvascular thrombosis as well as edema were detected proximal and distal to the trauma. FCD was reduced in muscle and fat tissue. The numbers of rolling and adherent leukocytes were enhanced 5 minutes after trauma and throughout the observational period.

Our results demonstrate endothelial leakage and extravasation early after low-energy soft tissue trauma in all soft tissues proximal and distal to the site of trauma. In addition, we found high accumulation of leukocytes in all locations, especially in soft tissues. The model presented is ideally suited for the in vivo investigation of new therapeutic strategies for edema and thrombosis prevention in animals with soft tissue trauma.