期刊
【作者单位】
="Department of Orthopedic Surgery Konig Ludwig Haus Julius-Maximilians-Universitat Wurzburg Brettreichstr. 11 97074 Wurzburg Germany. s-radke.klh@mail.uni-wuerzburg.de"
摘要 :
Transient bone marrow edema syndrome (TMES) is a rare disease of unknown etiology. Diagnosis is made by exclusion. There is still controversy as to whether TMES is considered to be a reversible form of avascular necrosis (AVN), a ...
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Transient bone marrow edema syndrome (TMES) is a rare disease of unknown etiology. Diagnosis is made by exclusion. There is still controversy as to whether TMES is considered to be a reversible form of avascular necrosis (AVN), a disease entity of its own or a form of non-traumatic algodystrophy. We here describe the extremely rare occurrence of three cases of TMES that progressed to AVN.
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摘要 :
Between 1990 and 2000, we treated 43 patients with transient bone marrow oedema of the hip. Five were treated with nonsteroidal antiinflammatory drugs (NSAIDs) and limited weight bearing, and 38 by core decompression followed by l...
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Between 1990 and 2000, we treated 43 patients with transient bone marrow oedema of the hip. Five were treated with nonsteroidal antiinflammatory drugs (NSAIDs) and limited weight bearing, and 38 by core decompression followed by limited weight bearing. At follow-up 2-10 years later, all patients were assessed by a structured interview as well as the Harris hip score (HHS) and the Western Ontario and MacMaster Universities Osteoarthritis Index (WOMAC). Both groups reached the same clinical outcome (HHS and WOMAC). Core decompression enabled a significantly faster recovery. There were no complications, but progression to avascular necrosis was seen in both groups. Core decompression induced fast pain relief, making it the preferable treatment.
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BACKGROUND: Transient marrow edema syndrome (TMES) of the hip is a disease of acute onset and severe functional disability. There is histological evidence for an ischemic etiology of TMES of the hip. Core decompression as applied ...
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BACKGROUND: Transient marrow edema syndrome (TMES) of the hip is a disease of acute onset and severe functional disability. There is histological evidence for an ischemic etiology of TMES of the hip. Core decompression as applied for avascular necrosis (AVN) of the hip is therefore a therapeutic alternative to conservative therapy, the latter leading only to a reduction of symptoms but never a shortening of the course of the disease. METHODS: Between January 1998 and June 2000, 22 hips with TMES were treated with core decompression in our department. TMES was diagnosed by exclusion. MRI was done preoperatively and at 6 months postoperatively. The postoperative MRI result was classified into three categories. RESULTS: After an average of 7.2 (range 1-30) days, all patients were pain-free after core decompression. In 2 patients, TMES progressed to AVN despite core decompression. All others had no signal alterations of the head of the femur on MRI after 6 months. The postoperative Harris Hip Score (HHS) in patients with TMES was on average 93.7 (range 77-95); in patients with AVN, the postoperative HHS was 47 (range 45-49). CONCLUSION: Our results demonstrate that core decompression of the hip significantly shortens the natural course of disease of TMES of the hip.
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We report a case of a sternal osteoid osteoma in a 39-year-old man. This localization is very rare and to our knowledge not described in literature.
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We performed a randomized, prospective study on the prophylaxis of heterotopic ossification (HO) after total hip arthroplasty (THR), comparing indomethacin and the selective COX-2 inhibitor meloxicam. From the day after surgery, 2...
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We performed a randomized, prospective study on the prophylaxis of heterotopic ossification (HO) after total hip arthroplasty (THR), comparing indomethacin and the selective COX-2 inhibitor meloxicam. From the day after surgery, 272 patients were treated with 7.5 mg meloxicam, 15 mg meloxicam, or 2 x 50 mg indomethacin a day, for 14 days. After 6 months, radiographs of patients treated with 7.5 mg meloxicam showed that HO had occurred in one third. This treatment was therefore stopped after 26 patients have been assigned to this group. According to the intention-to-treat principle, patients given 15 mg meloxicam developed HO in 25% (20% Brooker grade I, 4% grade II and 1% grade III) and those given indomethacin in 10% (7% Brooker grade I, 1% grade II and 2% grade III), a statistically significant difference.
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Wear particles are believed to induce periprosthetic inflammation which contributes to periprosthetic osteolysis. TNFalpha plays a pivotal role in the pathogenesis of this process. The molecular mechanisms leading to the developme...
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Wear particles are believed to induce periprosthetic inflammation which contributes to periprosthetic osteolysis. TNFalpha plays a pivotal role in the pathogenesis of this process. The molecular mechanisms leading to the development of periprosthetic inflammation with upregulated TNFalpha expression in monocytic cells in response to different wear particles have yet to be defined. In this study we evaluated the effects of polyethylene- and TiAlV-particles on activation of NF-kappaB signalling pathways and TNFalpha biosynthesis and release in monocytic cells with respect to periprosthetic osteoclastogenesis. THP-1 monocytic cells were differentiated to macrophage-like cells and exposed to LPS-detoxified polyethylene and prosthesis-derived TiAlV-particles. TNFalpha release was analyzed in culture supernatant by ELISA. NF-kappaB activation was examined by electrophoretic mobility shift assay (EMSA), and NF-kappaB target promoter activities including transactivation of the TNFalpha promoter were determinedby luciferase reporter gene assays. Differentiated THP-1 macrophages were exposed to increasing numbers of particles for 0, 60, 180 and 360 min. Both, polyethylene- and TiAlV-particles induced a significant activation of both NF-kappaB and TNFalpha promoters at 180 min. A significant TNFalpha release was detected after 360 min exposure to polyethylene- and TiAlV-particles in a dose dependent manner. In comparison, LPS induced a much greater activation of NF-kappaB and TNFalpha promoters, and TNFalpha secretion into the supernatant was strongly induced. These results provide evidence that induction of the NF-kappaB signal transduction pathway in macrophages plays a major role in initiating and mediating the inflammatory response leading to periprosthetic osteolysis.
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BACKGROUND: Wear debris has been associated with periprosthetic osteolysis and loosening of total joint arthroplasties. RANKL (receptor activator of NF-kappaB ligand), RANK (receptor activator of NF-kappaB) and OPG (osteoprotegeri...
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BACKGROUND: Wear debris has been associated with periprosthetic osteolysis and loosening of total joint arthroplasties. RANKL (receptor activator of NF-kappaB ligand), RANK (receptor activator of NF-kappaB) and OPG (osteoprotegerin) are three key molecules which regulate differentiation, survival, fusion, and activation of osteoclasts. MATERIAL AND METHODS: We evaluated the effect of TiAIV and polyethylene particles on expression of RANK, RANKL and OPG mRNA. We used a human monocytic leukemic cell line (THP-1) in this in vitro study. THP-1 monocytes were differentiated into macrophage-like cells and exposed to polyethylene particles and prosthesis-derived TiAIV particles. The supernantant was used for measurement of TNFalpha protein and total RNA was extracted from the cells. Expression of the genes coding for OPG, RANKL and RANK was analysed at the mRNA level using a semiquantitative RT-PCR method. RESULTS: Both polyethylene and TiAIV particles induced a significant release of TNFalpha after 6 h of exposure and a significant upregulation of RANK mRNA. OPG mRNA expression was transiently upregulated after exposure to polyethylene and TiAIV particles. These effects were dependent on particle dose. RANKL mRNA was not detectable in our THP-1 model. In contrast, LPS exhibited a different pattern of RANK/ RANKL/OPG mRNA expression. INTERPRETATION: Our findings provide evidence that both polyethylene and TiAIV particles induce upregulation of RANK expression in cells of the monocytic lineage, which may be important for periprosthetic osteoclastogenesis.
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