ObjectiveTo evaluate the effect of leucocyte- and platelet-rich plasma (L-PRP) on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) in treating avascular necrosis of the femoral head (ANFH) in rabbits. MethodsTwenty-four New Zealand white rabbits (4-6 months old, both genders, weighing 2.0-3.0 kg) were used for the establishment of bilateral ANFH models and divided into 4 groups (n=6). BMSCs were isolated from the bone marrow of iliac crest, cultured and identified. L-PRP was prepared by Landesberg method. Core decompression only (group A), core decompression and L-PRP implantation (group B), core decompression and BMSCs implantation (group C), and core decompression and implantation of BMSCs and L-PRP were performed in 4 groups. To evaluate bone formation and remodeling of the defects, X-ray photography was taken at 2, 4, and 8 weeks postoperatively. The modified Lane-Sandhu scoring system was used to evaluate the bone formation. Two rabbits were sacrificed at 2, 4, 8 weeks after operation to harvest the specimens for histological observation, new blood vessel count and new bone area ratio. ResultsThe observations of radiology and histology displayed different degrees of bone regeneration at bone defect sites in each group. At 2, 4, and 8 weeks postoperatively, the results of Lane-Sandhu X-ray photography scoring, new blood vessel count, and new bone area ratio showed that groups C and D were significantly better than groups A and B, group D was significantly better than group C. and group B was significantly better than group A (P<0.05). ConclusionThese findings demonstrate that L-PRP can promote osteogenic differentiation of BMSCs in treating ANFH in rabbits, and core decompression associated with BMSCs and L-PRP is an effective and feasible method to treat ANFH.
ObjectiveTo investigate the technique and short-term effectiveness of the umbrella-shaped memory alloy femoral head support device (umbrella-shaped support device for short) for the treatment of avascular necrosis of femoral head (ANFH). MethodsThe umbrella-shaped support device was fabricated with Ni-Ti alloy, and its biomechanics characteristics were tested by three-dimensional finite element analysis with pro/mechanica software. Between October 2009 and December 2012, 10 patients (18 hips) with ANFH were treated. There were 7 males (12 hips) and 3 females (6 hips), aged 21-53 years (mean, 40.6 years). The disease duration was 1-5 years (mean, 3.3 years). According to Ficat staged criteria, 10 hips were rated as stage Ⅱ, 6 hips as stage Ⅲ, and 2 hips as stage IV. Microtrauma methods were used to erase the necrotic tissue of the femoral head, and the umbrella-shaped support device, autogenous iliac bone graft, and artificial bone were implanted to support the collapsed femoral head. ResultsThree-dimensional finite element analysis showed that the largest stress of umbrella-shaped support device was 1 500 MPa and the largest displacement was 1.75 mm. Operation was successfully completed in the other 10 patients (17 hips) except 1 failure hip (total hip arthroplasty was performed after 6 months). The average follow-up period was 19.7 months (range, 15-26 months). At last follow-up, the results were excellent in 5 hips, good in 9 hips, fair in 2 hips, and poor in 1 hip; the excellent and good rate was 82.35%. The Ficat stage had no change when compared with preoperative stages. ConclusionThe advantages of the umbrella-shaped support device for the treatment of ANFH are to thoroughly remove the sequestrum, to rebuild blood circulation of the femoral head, to increase the machinery supporting of subchondral bone in weight-bearing area of femoral head, and to decrease the localized stress, and it has good short-term effectiveness, but long-term effectiveness needs further observation.
Objective To study the expression changes of vascular endothel ial growth factor (VEGF), basic fibroblast growth factor (bFGF), and bone morphogenetic protein 2 (BMP-2) in femoral neck fracture, traumatic, and non-traumatic avascular necrosis of femoral head (ANFH), and to study the relationshi p between the expressions of VEGF, bFGF, BMP-2mRNA and bone mass so as to explore the pathogenesis of ANFH and provide the exprimental basis for individual treatment of ANFH. Methods Femoral head specimens were obtained from 59 donors undergoing total hip replacement, including 22 cases of traumatic ANFH (group A, 13 cases of Ficat stage III and 9 cases of Ficat stage IV), 19 cases of non-traumatic ANFH (group B, 11 cases of Ficat stage III and 8 cases of Ficat stage IV; 10 cases of steroid-induced ANFH, 7 cases of alcohol ic ANFH, and 2 cases of unexplained ANFH), and 18 cases of fresh femoral neck fracture (group C). There was no significant difference in the general data among 3 groups (P gt; 0.05). The bone mineral density (BMD) at weight-bearing area of the femoral head was measured with dual energy X-ray absorptiometry. The pathological changes were observed by using optical microscope and scanning electron microscope. The percentage of empty bone lacuna and the percentage of trabecular bone area were calculated. The expressions of VEGF, bFGF, and BMP-2 mRNA in femoral head were detected by use of in-situ hybridization technique. Results The BMD in groups A and B were significantly lower than that in group C (P lt; 0.05), and there was significant difference between group A and group B (P lt; 0.05). In the necrosis area of groups A and B, the bone trabecula was rarefactive and not of integrity, with a great number of empty bone lacuna. In healthy area, more fiber hyperplasia was observed in group A, the prol iferated and hypertrophic fat cells in the medullary cavity in group B. Scanning electron microscope showed that many osteocytes underwent fatty degeneration and necrosis, and that the prol iferation of fat cells in bone matrix was observed in groups A and B. While in group C, the femoral head had intact articular cartilage and intact bone trabeculae, and osteocytes were clearly seen. The percentage of empty bone lacuna was significantly higher (P lt; 0.05) and the percentage of trabecular bone area was significantly lower (P lt; 0.05) in groups A and B than group C; and there was significant difference in the percentage of empty bone lacuna between groups A and B (P lt; 0.05). The expressions of VEGF, bFGF, and BMP-2 mRNAwere significantly lower in groups A and B than group C (P lt; 0.05), and the expressions of BMP-2 and bFGF mRNA in group A were significantly higher than those in group B (P lt; 0.05). There were positive l inear correlation between the expressions of VEGF mRNA, bFGF mRNA, BMP-2 mRNA and the BMD and percentage of trabecular bone area, respectively. While there were significantly negative correlation between the expressions of VEGF mRNA, bFGF mRNA, BMP-2 mRNA and percentage of empty bone lacuna. Conclusion The repair capacity of local femoral head in traumatic ANFH is ber than that in non-traumatic ANFH. The expressions of VEGF mRNA, bFGF mRNA, and BMP-2 mRNA decl ine in traumatic and nontraumatic ANFH.
【Abstract】 Objective To investigate corresponding relation between structure change of the femoral head with“crescent sign” and stress exerted on the avascular necrosis of femoral head, to explore the mechanism of the “crescent sign” formation. Methods From March 1998 to April 2003, the femoral heads of 18 hips in 16 cases having osteonecrosis and “crescent sign” in X-ray film before total hi p arthroplasty, were collected. General and coronal section plane morphology of the femoral heads were observed. The princi ple of effective stress and stress concentration theory were used to explain the phenomena and structure changes in osteonecrosis of the femoral head. Results Cancellous bone existed as a threedimensional,interconnected network of trabeculae rods and plates, with 50%-90% of porosity and 20-30 mmHg bone marrow pressure. According to the definition of porous media, bones especially cancellous bone was a kind of sol id and l iquid two phases porous media. Cross-sectional structure changes in the junction between subchondral plate and cancellous were the place where stress concentrated. The principle of effective stress and stress concentration theory could explain the phenomena and their relationship that occurred in avascular necrosis of the femoral head. Conclusion The “crescent sign” starts in an area of very focal resorption in the subchondral plate laterally and peripherally. The focal resorption in the subchondral plate breaks the continuity of subchondral plate and causes stress concentration in the resorption region. The concentrated stress accumulates in the junction between subchondral plate and unrepaired necrotic cancellous bone brings on the fracture right below the subchondral plate. The focal resorption of the subchondral plate also provides a pathway for the pore water in the unrepaired necrotic bone skeleton to outflow, therefore cause effective stress increase and unrepaired necrotic bone skeleton be compacted by increased effective stress appl ied on unrepaired necrotic cancellous bone skeleton, and results in the volume decrease of unrepaired necrotic cancellous bone and the formation of cavum below the subchondral plate. The cavum shows “crescent sign” in the X-ray film.
【Abstract】 Objective To investigate the spectrum of CT and MR imaging and surgical operation findings in il iopsoasbursitis in patients with avascular necrosis of femoral head so as to enhance the diagnostic abil ity. Methods A total of 1 415 patients with avascular necrosis of the femoral head were analyzed retrospectively; of them, 15 patients were compl icated by il iopsoas bursitis surgically or aspiration of synovial fluid between May 2005 and May 2007. Fifteen cases were all necrosis of the bilateral femoral head and 17 hips were combined with il iopsoas bursitis. There were 14 males and 1 female, aging 29-58 years. The course of disease was 1 month to 3 years. All 15 patients had l imitation of abil ity of the hips and the “4” type sign was positive. The Harris score of hip’s function was 54-78 (mean 62.7). Five patients of them can be touched a palpable cystic mass and tenderness in the inguinal area, and 3 of them associated with femoral neuropathy and 2 patients presented sl ight atrophy of the thigh muscle in suffering side. All these cases were taken X-ray films of positive and frog-leg lateral position, hel ical CTscan with 5 mm thinness, and MRI was performed in 6 patients with T1WI, T2WI, T2WI and fat-saturated inversion recovery sequence. Results The radiographs were the primary basis evidences for diagnosis and degrees of the avascular necrosis of femoral head. According to the standards of Association Research Circulation Osseuse, there were 2 hips at stage II(II C 2), 6 hips at stage Ⅲ ( Ⅲ B 1, Ⅲ C 5 ) and 9 hips at stage IV. The X-ray films showed the bulging of the fat pad and soft tissue swell ing in 6 patients. CT analysis disclosed that the enlarged il iopsoas bursae appeared as hypodense, well-defined, thin-walled (lt; 2 mm) cystic structures. The content of the examined bursae was homogeneous with a CT density of ranging from 12.7 to 41.2 Hu, showing fluid collection. They were round or oval in shape medial to the il iopsoas, exhibiting inverted water-drop cystic shadow just inferior to the femoral head. Sl ight contrast enhancement of the bursal wall was seen after contrast agent administration in 3 cases. MRI demonstrated that the il iopsoas bursitis presented as low signal on T1WI and water-l ike highsignal on T2WI and markedly higher signal on STIR in 6 cases. The demonstration of the extent, size, mass effects and its relation and subsequent affection to surrounding anatomical structures were clearly shown by MRI, and by the communications between the il iopsoas bursa and the adjacent hip joint. Conclusion In the diagnosis of avascular necrosis of femoral head with imaging approaches, much attention should be paid to the abnormal ities around the articular capsule to early identify il iopsoas bursitis for further management.
Objective?To explore the difference between bone marrow edema syndrome (BMES) and avascular necrosis of femoral head (ANFH).?Methods?Recent original articles about BMES and ANFH were extensively reviewed, and were comprehensively analysed.?Results?The pathology, pathogenesis, clinical features, treatment selection, and prognosis are different between these two diseases.?Conclusion?BMES and ANFH are two different diseases. Micro-fracture may be the cause of bone marrow edema.
Objective?To investigate the effect of glucocorticoid on the expression levels of osteoprotegerin (OPG)/receptor activator of nuclear factor kappa B ligand (RANKL)-matrix metalloproteinases (MMP)/tissue inhibitor of matrix metalloproteinase (TIMP) system in bone tissues of femoral head of rats, and to discuss its interrelated action mechanism in glucocorticoid-induced avascular necrosis of femoral head (ANFH).?Methods?Forty adult Sprague Dawley rats, weighing 250-300 g, half males and half females, were randomly divided into 4 groups: high dose glucocorticoid group (HD, n=10), medium dose glucocorticoid group (MD, n=10), low dose glucocorticoid group (LD, n=10), and control group (n=10). The rats in HD group, MD group, and LD group were intramuscularly injected with 25.0, 12.5, and 7.0 mg/kg of prednisolone respectively, and the rats in the control group were injected with physiological saline. After 4 weeks intervention, the osteonecrosis of left femoral heads was observed by HE staining, total RNA was extracted from the right femoral head bone tissue and the mRNA expression levels of OPG, RANKL, MMP-2, MMP-9, TIMP-1, and TIMP-2 were detected by RT-PCR.?Results?After injection of prednisolone, 4 rats of HD group and 1 rat of MD group died of systemic failure caused by the decreased food and weight culminating in cachexia. HE staining showed that the integrity of bone trabecula and osteon was destroyed at different levels, discontinuous bone chips formed, and osteocytes were replaced by granulation tissue in some lacunae in HD, MD, and LD groups; the integrated osteon was observed, the lamellar structure formed concentric circles around the blood vessel and osteocytes were seen in the lacunae in the control group. The necrosis rates of femoral head were 83.3% (5/6), 66.7% (6/9), 30.0% (3/10), and 0 (0/10) in HD, MD, LD, and control groups. The results of RT-PCR showed: the mRNA expression levels of the OPG, TIMP-1, TIMP-2 in HD, MD, and LD groups were lower than those in the control group, showing significant differences (P lt; 0.05) and there was negative correlation with the hormone dosage. The difference in OPG expression was significant between the hormone groups (P lt; 0.05); the differences in the TIMP-1 and TIMP-2 expressions were not significant between the LD group and MD group (P gt; 0.05), but there were significant differences when compared with HD group (P lt; 0.05). The RANKL, MMP-2, and MMP-9 mRNA expression levels in HD, MD, and LD groups were higher than those in the control group and there was a positive correlation with the hormone dosage, showing significant differences when compared MD and HD groups with control group (P lt; 0.05); there was no significant difference in RANKL expression between HD group and MD group (P gt; 0.05), but there was significant difference when compared HD and MD groups with LD group (P gt; 0.05); no significant difference was observed in the MMP-2 and MMP-9 expression between MD group and LD group (P gt; 0.05), but the differences were significant when compared with HD group (P lt; 0.05).?Conclusion?Glucocorticoid-induced ANFH may be related to the expression levels of OPG/RANKL-MMP/TIMP mRNA regulated by glucocorticoid.
Objective Glucocorticoid is the main cause of non-traumatic avascular necrosis of femoral head. To explore the changes of reactive oxygen species (ROS) in the bone microvascular endothel ial cells treated with glucocorticoid so as to investigate the pathogenesis of steroid-induced avascular necrosis of femoral head. Methods The cancellous bone of femoral head was harvested from voluntary donators undergoing total hip arthroplasty, and then the bone microvascular endothel ial cells were isolated by enzyme digestion. The cells at passage 3 were cocultured with different concentrations of hydrocortisone (0, 0.03, 0.10, 0.30, and 1.00 mg/mL) for 24 hours. MTT assay was used for the inhibitory rate of cell prol iferation, flow cytometry for apoptosis rate, and fluorescence probe for the production of ROS and xanthine oxidase (XOD). Results At 2-3 days primary culture, the cells were spindle and arranged l ike cobbles and they reached confluence after 1 week. The inhibitory rates of cell prol iferation in 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 20.22% ± 2.97%, 22.94% ± 4.52%, 43.98% ± 3.35%, and 78.29% ± 3.85%, respectively; and 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 2 low-concentration groups (0.03 and 0.10 mg/mL groups). The apoptosis rates in 0, 0.03, 0.10, 0.30, and 1.00 mg/mL groups were 0.10% ± 0.01%, 0.23% ± 0.02%, 1.83% ± 0.04%, 6.34% ± 0.11%, and 15.33% ± 0.53%, respectively; 2 high-concentration groups (0.30 and 1.00 mg/mL groups) were significantly higher (P lt; 0.05) than 0 mg/mL group. In 0, 0.30, and 1.00 mg/ mL groups, the ROS levels were 57.35 ± 7.11, 120.47 ± 15.68, and 166.15 ± 11.57, respectively, and the XOD levels were 0.017 9 ± 0.000 9, 0.028 3 ± 0.001 7, and 0.067 7 ± 0.004 1, respectively; there were significant differences in the levels of ROS and XOD among 3 groups (P lt; 0.05). Conclusion Increasing of ROS production in bone microvascular endothel ial cells can be induced by high concentration glucocorticoid, and it can result in cell injury
Eight cases(10 hips) of avascular necrosis of femoral head in adults were treated with transplantation of sartorius musculo-skeletal graft through the greater trochanter since August 1990. The patients were followed up for 12 to 20 months,with disappearance of pain in 7 cases. The degree of hip motion was markedly increased. The good results rated 87.5 percent.
Objective To review the relationshi p between heritable hypercoagulable state (HHCS) and avascular necrosis of femoral head (ANFH). Methods The latest original articles about the relationshi p between HHCS and ANFH were extensively reviewed. Results Several genetic mutations which could cause HHCS, such as thrombophilic factor V G1691A gene, thrombophilic factor II G20210A gene, 5, 10-methylenetetrahydrofolate reductase C677T gene, plasminogen activator inhibitor 1 4G/5G, and tissue factor pathway inhibitor gene, may be genetic risks of ANFH. Conclusion HHCS may be a genetic cause of ANFH. Further studies are needed to confirm the relationship between HHCS and Chinese ANFH.