Omentin-1 promotes mitochondrial biogenesis via PGC1α-AMPK pathway in chondrocytes.

OBJECTIVE: Omentin-1 is a newly discovered metabolic regulatory adipokine. Studies have shown that omentin-1 possesses pleiotropic effects in different types of cells. This study aims to investigate the regulation by omentin-1 on mitochondrial biogenesis in chondrocytes. METHODOLOGY: C-28/I2 chondrocytes were treated with omentin-1 (150 and 300 ng/ml) for 24 h. The expression of mitochondrial regulators, markers and the DNA copy was assessed. The mitochondrial morphology was observed by electron microscopy. The mitochondrial respiratory rate and ATP production in chondrocytes were measured by cell lysates. RESULTS: Omentin-1 treatment up-regulated PGC-1α, NRF-1 and mitochondrial transcription factor A (TFAM) in cultured chondrocytes, indicating that omentin-1 could be involved in the regulation of mitochondrial function. Omentin-1 promoted mtDNA/nDNA and four mitochondrial genes (Tomm20, Tomm40, Timm9 and Atp5c1), mRNA transcripts as well as two mitochondrial protein expressions (SDHB and MTCO1). At a cellular level, omentin-1 enhanced the mitochondrial respiratory rate and ATP production. Mechanistically, we proved that omentin-1 increased AMPKα activation, and the blockage of AMPKα by its inhibitor compound C abolished the inductive effect of omentin-1 on PGC1α expression and mtDNA/nDNA ratio, indicating that the effect of omentin-1 is dependent on AMPKα activation. CONCLUSION: Omentin-1 is a positive regulator of mitochondrial biogenesis in chondrocytes, and its action is dependent on the AMPK-PGC1α pathway. This study, therefore, implies that omentin-1 has the potential to remedy chondrocyte damage in the prevention and treatment of osteoarthritis.

Correlation of Multiple Acromion Morphological Parameters on Radiographs in a Geriatric Chinese Population and Its Clinical Significance.

INTRODUCTION: Previous clinical studies have reported associations between the acromion index, lateral acromion angle, and critical shoulder angle and the occurrence of rotator cuff tears. The objective of this study was to analyze the correlations of these different anatomic parameters in geriatric Chinese Population. METHODS: Healthy geriatric Chinese participants (n = 66) and geriatric Chinese patients with rotator cuff tears (n = 70) identified between January 2019 and October 2020 were included in this study. Standardized true anteroposterior radiographs were used to measure the acromion index, lateral acromion angle, and critical shoulder angle in each study participant. RESULTS: The mean acromion index was significantly larger, the mean lateral acromion angle was significantly smaller, and the mean critical shoulder angle was significantly larger in geriatric patients with full-thickness rotator cuff tears compared with geriatric healthy participants. CONCLUSION: There were a negative linear relationship between the acromion index and lateral acromion angle and a positive linear relationship between the acromion index and critical shoulder angle in geriatric patients with rotator cuff tear and geriatric healthy participants; we termed this phenomenon "Hypothesis of Acromion Index." The acromion index, lateral acromion angle, and critical shoulder angle are independent predictors of rotator cuff tears in a geriatric Chinese population.

Basic fibroblast growth factor and agarose gel promote ​the ability of immune privilege of allogeneic cartilage transplantation in rats.

OBJECTIVE: Allogeneic cartilage transplantation is used to treat severe osteochondral defects or cartilaginous injury. However, acute immune rejection has been a key problem interfering with graft healing. METHODS: Full-thickness osteochondral defects were performed in Sprague Dawley rats. The allograft implants were set into the defect region. Blood and spleen samples from Postoperative Day 3 onward were collected for inflammatory cell analysis, including analysis of monocytes, natural killer cells, CD4+CD25+Foxp3+ regulatory T cells, CD4+ T cells, and CD8+ T cells. Gross observation and histologic staining (hematoxylin and eosin, toluidine blue) were carried out at the same time point to assess the repair effect of the cartilage graft and the degree of immune rejection. RESULTS: Treatment with basic fibroblast growth factor, agarose gel, and allogeneic cartilage was similar to that of the autologous group. The percentage of monocytes in allografts was at a higher level in the spleen and blood; the frequency of CD4+ T cells in the allogeneic group was higher than in the autologous group and the other agarose groups at 6 weeks after transplantation. The number of regulatory T cells in the autograft was increased from Postoperative Week 1; similar results were observed in groups containing basic fibroblast growth factor beginning at Postoperative Week 3. CONCLUSIONS: Allogeneic cartilage transplantation induces acute immune rejection, which compromises the validity of the implant. The combination of basic fibroblast growth factor and agarose gel facilitates the goal of immune privilege and promotes the success of the allograft tissues. THE TRANSLATIONAL POTENTIAL OF THIS ARTICLE: This study investigated the combination of basic fibroblast growth factor (bFGF) and agarose gel facilitates promotes the success of the allograft tissues transplantation. This work may help clinicians find a new way to repair articular cartilage damage. This will affect the treatment of articular cartilage movement injuries and arthritis.

Effects of receptor activator nuclear factor κB gene polymorphisms on the susceptibility to knee osteoarthritis: A case-control study.

The present study aimed to explore genetic association of receptor activator nuclear factor κB (RANK) polymorphisms with individual susceptibility to knee osteoarthritis (OA) in different Kellgren-Lawrence (KL) grades.This case-control study included 138 knee OA patients and 145 healthy individuals. RANK rs1805034 and rs8086340 polymorphisms were genotyped through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The effects of RANK polymorphisms on knee OA risk were analyzed via χ test or Fisher exact test, and the results were expressed using odds ratios (ORs) with corresponding 95% confidence intervals (CIs).The C allele of rs1805034 polymorphism had significantly higher frequency in knee OA patients than in controls (P = .044), indicating that this allele could increase the risk of knee OA (OR = 1.424, 95% CI = 1.010-2.008). Besides, the CC genotype and C allele of the rs1805034 polymorphism were significantly associated with elevated risk of knee OA in moderate grade (CC vs TT: P = .018, OR = 3.071, 95% CI = 1.187-7.941; C vs T: P = .012, OR = 1.787, 95% CI = 1.131-2.823). However, rs8086340 polymorphism had no significant association with knee OA riskThe C allele of RANK rs1805034 polymorphism is closely correlated with increased risk of knee OA, especially for moderate grade.

MiR-300 Serves as Potential Biomarker to Screen Knee Osteoarthritis Patients by Targeting TNFα.

BACKGROUND: This study mainly explored the serum level of miR-300 with the risk of knee OA, thereby evaluating their diagnostic ability for treatment of knee osteoarthritis (KOA) patients. METHODS: In the current study, we evaluated the level of TNFα in KOA patients and HCs. The serum was used to quantify the level of TNF-α by way of a sandwich enzyme-linked immunosorbent assay. Dual luciferase reporter assay was carried out to identify the possible target gene of miR-300. RESULTS: In line with previous studies, our data showed that serum TNFα level was increased along with K/L grades and WOMAC scoring, suggesting TNFα induced inflammatory responses correlating with the severity of KOA. We also showed that serum miR-300 level was increased with the severity of KOA according to X ray examination and K/L grades. Furthermore, we showed that serum miR-300 level positively correlated with K/L grades, Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain scoring and WOMAC function scoring. Bioinformatic predictions showed a conserved binding site of miR-300 in the 3'UTR of IκBα. We then carried out a dual luciferase reporter assay and found miR-300 significantly suppressed pmirGLO-IκBα-3'UTR luciferase activity. CONCLUSIONS: Serum miR-300 is increased with the severity of KOA according to X-ray examination and K/L grades, thereby reflecting the severity of KOA and the degree of cartilage damage. Therefore, it could be used as a potential biomarker to screen KOA patients from healthy controls.

Interferon regulatory factor 5 (IRF5) regulates the expression of matrix metalloproteinase-3 (MMP-3) in human chondrocytes.

Matrix metalloproteinase-3 (MMP-3) plays a pivotal role in the destruction of articular cartilage in osteoarthritis (OA). The regulation of gene expression of MMP-3 is complicated. Interferon regulatory factor 5 (IRF5) is a member of the interferon regulatory factor family of transcription factors. Little information regarding the biological function of IRF5 on chondrocytes and the pathogenesis of OA has been reported. In the current study, for the first time, we report that IRF5 is expressed in human primary chondrocytes and human chondrosarcoma cell line SW1353 cells. In addition, IRF5 is upregulated in response to TNF-α treatment in a dose dependent manner. Interestingly, IRF5 is significantly higher in chondrocytes from OA patients compared to those from normal subjects. Notably, IRF5 mediates TNF-α- induced expression of MMP-3 in chondrocytes. Overexpression of IRF5 promotes the expression of MMP-3, however, knockdown of IRF5 reduces the expression of MMP-3. Mechanistically, IRF5 is able to enhance the transcription of MMP-3 by binding to its promoter. Also, we found that NF-κB was involved in the effects of IRF-5 on MMP-3 expression. These findings suggest that IRF5 might be a novel pharmacological target for the treatment of OA and RA.

Protective effects of Nebivolol against interleukin-1ß (IL-1ß)-induced type II collagen destruction mediated by matrix metalloproteinase-13 (MMP-13).

The pathological progression of osteoarthritis (OA) involves degradation of articular cartilage matrix. Type II collagen is the main component of cartilage matrix, which is degraded by pro-inflammatory cytokines such as IL-1ß mediated by MMP-13. Nebivolol, a licensed drug used for the treatment of hypertension in clinics, displays its anti-inflammatory capacity in various conditions. However, whether Nebivolol has a protective effect on cartilage matrix degradation has not been reported before. In this study, we investigated the effects of Nebivolol on regulating the expression of MMP-13 and degradation of type II collagen. Our results indicate that Nebivolol alleviated the increase in gene expression, protein expression, and activity of MMP-13 induced by IL-1ß. Importantly, IL-1ß strikingly reduced the levels of type II collagen in cell culture supernatants, which was reversed by treatment with Nebivolol in a dose-dependent manner. Mechanistically, Nebivolol was found to alleviate the increased levels of phosphorylated IκBα and reduced levels of total IκBα induced by IL-1ß, which subsequently mitigated p65 nuclear translocation and the transcriptional activity of NF-κB. Furthermore, our results indicated that IL-1ß treatment resulted in a significant increase in expression of the transcriptional factor interferon regulatory factor-1 (IRF-1) at both the mRNA and protein levels, which was significantly ameliorated by treatment with Nebivolol. The combination of these findings suggests that Nebivolol can potentially be applied in human OA treatment.

Prevalence of Developmental Dysplasia of the Hip in Chinese Adults: A Cross-sectional Survey.

BACKGROUND: The prevalence of developmental dysplasia of the hip (DDH) is unknown in China. We aimed to determine the prevalence of DDH in Chinese adults. METHODS: In this study, we performed a cross-sectional survey of a nationally representative sample of Chinese adults. All participants underwent questionnaire investigation, physical examination, and X-ray examination. Factors associated with DDH were analyzed with logistic regression. RESULTS: We invited 29,180 individuals aged 18 years and over to participate, randomly selected from 18 primary sampling units (street districts in urban areas and townships in rural areas). The survey and examination were completed in 25,767 people (10,296 men and 15,471 women). DDH was diagnosed in 391 people, yielding an overall DDH prevalence of 1.52%. Based on this information, we estimate the number of individuals with DDH in China to be approximately 16.05 million. DDH prevalence increased with age (odds ratio = 1.53 [1.03-2.27], P = 0.036), was significantly higher among women than men (2.07% vs. 0.75%, P< 0.001), and was higher among rural residents than urban residents (1.75% vs. 1.29%, P< 0.001). Economic development was independently associated with the presence of DDH. There was no evidence of an association between body mass index alone, education, or current smoking or drinking and risk of DDH (P > 0.05). CONCLUSIONS: DDH has become an important public health problem. Special attention should be paid to residents with DDH. Screening for DDH should be performed in China.

Omentin-1 prevents cartilage matrix destruction by regulating matrix metalloproteinases.

Matrix metalloproteinases (MMPs) play a crucial role in the degradation of the extracellular matrix and pathological progression of osteoarthritis (OA). Omentin-1 is a newly identified anti-inflammatory adipokine. Little information regarding the protective effects of omentin-1 in OA has been reported before. In the current study, our results indicated that omentin-1 suppressed expression of MMP-1, MMP-3, and MMP-13 induced by the proinflammatory cytokine interleukin-1ß (IL-1ß) at both the mRNA and protein levels in human chondrocytes. Importantly, administration of omentin-1 abolished IL-1ß-induced degradation of type II collagen (Col II) and aggrecan, the two major extracellular matrix components in articular cartilage, in a dose-dependent manner. Mechanistically, omentin-1 ameliorated the expression of interferon regulatory factor 1 (IRF-1) by blocking the JAK-2/STAT3 pathway. Our results indicate that omentin-1 may have a potential chondroprotective therapeutic capacity.

Identification of dysregulated genes in rheumatoid arthritis based on bioinformatics analysis.

BACKGROUND: Rheumatoid arthritis (RA) is a chronic auto-inflammatory disorder of joints. The present study aimed to identify the key genes in RA for better understanding the underlying mechanisms of RA. METHODS: The integrated analysis of expression profiling was conducted to identify differentially expressed genes (DEGs) in RA. Moreover, functional annotation, protein-protein interaction (PPI) network and transcription factor (TF) regulatory network construction were applied for exploring the potential biological roles of DEGs in RA. In addition, the expression level of identified candidate DEGs was preliminarily detected in peripheral blood cells of RA patients in the GSE17755 dataset. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to validate the expression levels of identified DEGs in RA. RESULTS: A total of 378 DEGs, including 202 up- and 176 down-regulated genes, were identified in synovial tissues of RA patients compared with healthy controls. DEGs were significantly enriched in axon guidance, RNA transport and MAPK signaling pathway. RBFOX2, LCK and SERBP1 were the hub proteins in the PPI network. In the TF-target gene network, RBFOX2, POU6F1, WIPF1 and PFKFB3 had the high connectivity with TFs. The expression status of 11 candidate DEGs was detected in GSE17755, the expression levels of MAT2A and NSA2 were significantly down-regulated and CD47 had the up-regulated tendency in peripheral blood cells of patients with RA compared with healthy individuals. qRT-PCR results of MAT2A, NSA2, CD47 were compatible with our bioinformatics analyses. DISCUSSION: Our study might provide valuable information for exploring the pathogenesis mechanism of RA and identifying the potential biomarkers for RA diagnosis.

Carvedilol suppresses cartilage matrix destruction.

Collagen type Ⅱ (col Ⅱ) and aggrecan, the main components of the extracellular matrix (ECM) in human joint cartilage, have been reported to be reduced by chronic production of inflammatory cytokine interleukin (IL)-1ß in arthritic joints. Carvedilol, a licensed medicine, has been used for treatment of hypertension, congestive heart failure and coronary disease in clinics. In this study, we investigated the effects of Carvedilol on the expression of col Ⅱ and aggrecan. Our results demonstrate that treatment with Carvedilol didn't change the expression of aggrecan or col Ⅱ at mRNA levels in SW1353 chondrocytes. However, the expression of aggrecan and Col II at protein levels were significantly reduced by IL-1ß treatment, which were reversed by Carvedilol in a dose dependent manner, suggesting the inhibitory effects of Carvedilol on the expression of aggrecan and Col II are at post-translational modification levels. In addition, it was shown that IL-1ß treatment highly induced MMP-1 and MMP-13 expression in SW1353 chondrocytes at both gene and protein expression levels, which were restored by Carvedilol in a dose dependent manner. Mechanistically, exposure to IL-1ß increased phosphorylation of IKK-α/ß and degradation of IκB-α in SW1353 chondrocytes, which were suppressed by pretreatment with Carvedilol. Administration of Carvedilol inhibited IL-1ß-induced translocation of NF-κB p65 from cytosol to nucleus manner. Notably, a luciferase reporter assay showed that IL-1ß severely increased NF-κB luciferase activity, which was markedly suppressed by Carvedilol treatment. Our results suggest that Carvedilol might be a potential therapeutic agent for chondro-protective therapy.

An insertion/deletion polymorphism at the microRNA-122 binding site in the interleukin-1α 3'-untranslated region is associated with a risk for osteoarthritis.

Polymorphisms located at microRNA (miRNA) binding sites may affect the expression of genes. The present study aimed to identify the association between an insertion/deletion (Ins/Del) polymorphism (rs3783553) in the 3'­untranslated region (3'­UTR) of interleukin­1α (IL­1A) and the risk for osteoarthritis (OA). Using a luciferase reporter system, IL­1A was identified in the present study as an effective target gene of miR­122 in synovial cells that were obtained from patients who had received a synovectomy. This finding was verified further by the observation that exogenous over­expression of miR­122 in the synovial cells significantly downregulated the expression of IL­1A in the cells with Ins/Ins and Ins/Del genotypes, but not in the cells with Del/Del genotypes. Patients with OA (n=931) and OA­free volunteers (n=952) were enrolled in the study. Compared with the Del/Del genotype, patients possessing the Ins/Del or Ins/Ins genotype were associated with a lower risk for OA [odds ratio (OR)=0.67, P=0.0051; OR=0.65, P=0.0031, respectively], and the association was even stronger in young subjects (<62 years) (OR=0.53; P<0.001). Additionally, it was found that genotype was associated with radiographic severity (OR=0.72; P=0.023). The synovial fluid (SF) concentrations of IL­1A and miR­122 were measured in 75 OA patients. While the miR­122 concentrations were found to be comparable between each genotype group, the SF concentration of IL­1A in the Del/Del group was significantly higher than in the Ins/Del and Ins/Ins genotype groups. Therefore, the present study identified that the Ins/Del polymorphism in the 3'­UTR of IL­1A may affect genetic expression and, to the best of our knowledge, is the first study to demonstrate that the minor allele (Del) is associated with an elevated risk for OA and disease severity.

Analysis of single nucleotide polymorphisms within ADAM12 and risk of knee osteoarthritis in a Chinese Han population.

OBJECTIVE: Osteoarthritis (OA) is a complex arthritic condition in which the genetic factor plays a major role. One of the candidate genes of is the ADAM12 gene, but no consistency has been reached till now. This study aims to investigate the potential role of four single nucleotide polymorphisms (SNPs) of the ADAM12 gene in susceptibility to knee OA and its progression in Chinese Han population. METHODS: The rs1278279, rs3740199, rs1044122, and rs1871054 polymorphisms were genotyped and compared in a population based cohort consisting of 164 OA subjects and 200 age- and gender-matched controls. RESULTS: The SNP rs1871054 was found with increased risk of OA susceptibility in comparing the genotype frequencies between the case and control groups no matter for which model of comparison (allele level, dominant model, recessive model, and extreme genotype model). Additionally, the SNP rs1871054 was found associated with increased OA severity according to the K/L grade. CONCLUSION: In summary, we have identified that the rs1871054 variant within the ADAM12 gene is a risk factor for increased osteoarthritis susceptibility and severity.

Combined vascularized iliac and greater trochanter graftings for reconstruction of the osteonecrosis femoral head with collapse: reports of three cases with 20 years follow-up.

In this report, we present the long-term results of using combined vascularized iliac and greater trochanter graftings for reconstruction of the osteonecrosis of the femoral head (ONFH) with collapse in three patients. Necrosis over two-thirds of the femoral head and collapse were observed in these patients, with Harris hip scores (HHS) of 46, 38, and 49 points, respectively. When the patients underwent the femoral head reconstruction procedures, the ages of the patients ranged from 20 to 28 years old. The patients were followed-up for 20-24 years. X-ray examinations showed no progress of necrosis or deformity in the femoral head of patients after surgery, with the exception of bone absorption in one patient with persistence of mild pain. The HHS in the three patients were 84, 65, and 86 points at the end of follow-up, respectively. These results show that the vascularized iliac and greater trochanter graftings may be a valuable option for reconstruction of the ONFH with collapse in younger patients.

Treatment of early stage osteonecrosis of the femoral head with autologous implantation of bone marrow-derived and cultured mesenchymal stem cells.

BACKGROUND: Treatment of early-stage osteonecrosis of the femoral head (ONFH) with autologous implantation of iliac crest bone marrow-derived mononuclear cells, which contain tens of thousands of bone marrow mesenchymal stem cells (BMMSCs), recently achieved a promising outcome. METHODS: One hundred patients with early-stage ONFH were recruited and randomly assigned to BMMSC treatment or core decompression (CD) treatment. Each BMMSC-treated hip received femoral head (FH) implantation of 2×10(6) autologous subtrochanteric bone marrow-derived and ex vivo expanded BMMSCs. The radiographic stage of ONFH according to the Association Research Circulation Osseous classification, Harris hip score (HHS), and the volume of the necrotic lesion or the low signal intensity zone (LowSIZ) in the FH were assessed before and 6, 12, 24, and 60 months after the initial operation. RESULTS: Sixty months after the operation, only 2 of the 53 BMMSC-treated hips progressed and underwent vascularized bone grafting. In CD group, 7 hips lost follow-up, and 10 of the rest 44 hips progressed and underwent vascularized bone grafting (5 hips) or total hip replacement (5 hips). Compared with the CD group, BMMSC treatment significantly improved the HHS as well as decreased the volume of femoral head LowSIZ of the hips preoperatively classified at stage IC, IIB, and IIC (P<0.05, respectively; stage IIA, P=0.06, respectively). No complication was observed in both treatment groups. CONCLUSIONS: Ex vivo expansion of autologous BMMSCs can reliably provide a greater number of BMMSCs for FH implantation. This intervention is safe and effective in delaying or avoiding FH collapse, which may necessitate total hip replacement.

Inhibition of CYP3A4 and CYP2C9 by podophyllotoxin: implication for clinical drug-drug interactions.

Podophyllotoxin (PPT) and its derivatives exert significant anti-cancer activities, and one derivative etoposide is often utilized to treat various cancers in the clinic. The aim of the present study is to investigate the inhibitory effects of PPT on major cytochrome P450 (CYP) isoforms in human livers. Inhibition of CYP3A4, CYP2C9, CYP2C8, CYP2D6, CYP2E1 and CYP2A6 by PPT was investigated in the human liver microsomal system. Time-dependent inhibition of CYP3A4 by PPT was also evaluated. The results showed that PPT strongly exhibited inhibitory effects on CYP3A4 and CYP2C9 in a concentration-dependent manner. Half inhibition concentration (IC50) was 1.1 +/- 0.3 and 4.6 +/- 0.3 meu M for CYP3A4 and CYP2C9, respectively. Inhibition kinetic analysis showed that PPT exhibited competitive inhibition towards CYP3A4 and CYP2C9 with Ki of 1.6 and 2.0 meu M, respectively. Additionally, PPT exerted time-dependent inhibition towards CYP3A4 and the kinetic parameters were 4.4+/- 2.1 meu M and 0.06 +/- 0.01 min-1 for KI and kinact, respectively. Our experimental data indicate that potential drug-drug interaction (DDI) might exist when PPT is co-administered with the substrates which mainly undergo CYP3A4- or CYP2C9-mediated metabolism.

[Treatment of avascular necrosis of femoral head after femoral neck fracture with pedicled iliac bone graft].

OBJECTIVE: To explore the effectiveness of pedicled iliac bone graft transposition for treatment of avascular necrosis of femoral head (ANFH) after femoral neck fracture. METHODS: Between June 2002 and December 2006, 22 cases (22 hips, 16 left hips and 6 right hips) of ANFH after femoral neck fracture were treated with iliac bone graft pedicled with ascending branch of the lateral femoral circumflex vessels. There were 18 males and 4 females with an age range from 28 to 48 years (mean, 37.5 years). The time from injury to internal fixation was 2-31 days, and all fractures healed within 12 months after internal fixation. The ANFH was diagnosed at 15-40 months (mean, 22 months) after internal fixation. The ANFH duration was 3-11 months (mean, 8 months). According to Association Research Circulation Osseous (ARCO) staging system, 2 hips were classified as stage IIa, 3 hips as stage IIb, 3 hips as stage IIc, 3 hips as stage IIIa, 7 hips as stage IIIb, and 4 hips as stage IIIc. The preoperative Harris hip score (HHS) was 64.10 +/- 5.95. RESULTS: All incisions healed by first intention and the patients had no complication of lung embolism, sciatic nerve injury, lower limb deep venous thrombosis, and numbness and pain of donor site. All patients were followed up 2.5 to 6.3 years (mean, 4.8 years). The fracture healing time was 8-12 months, and no femoral neck fracture recurred. The HHS was 90.20 +/- 5.35 at last follow-up, showing significant difference when compared with the preoperative value (t = -18.447, P = 0.000). The hip function were excellent in 11 hips, good in 10 hips, fair in 1 hip, and the excellent and good rate was 95.5%. Four hips were radiographically progressed in ARCO staging, 18 hips remained stable with a stable rate of 81.8%. CONCLUSION: Pedicled iliac bone graft transposition is an ideal option for treatment of ANFH after internal fixation of femoral neck fracture for the advantages of femoral head revascularization, sufficient cancellous bone supply, and relatively simple procedure.

Will a vascularized greater trochanter graft preserve the necrotic femoral head?

BACKGROUND: Various head-preserving procedures have been used for young patients with osteonecrosis of the femoral head (ONFH) to avert the need for THA. However, none of these techniques are accepted universally because of the technical difficulties, complications, or mixed results that often are difficult to reproduce. QUESTIONS/PURPOSES: We describe a technique using vascularized bone grafting for treating ONFH in Stages II-IV (Ficat and Arlet) disease, describe our indications, and report the survival of this technique and the functional scores. METHODS: We retrospectively reviewed 191 patients (195 hips) who underwent vascularized greater trochanter grafting for osteonecrosis of the femoral head (Ficat and Arlet Stages II-IV) from 1995 to 2006. The mean age of the patients was 44 years (range, 19-59 years). The minimum followup was 2 years (mean, 8 years; range, 2-11 years). RESULTS: Twenty patients (23 hips) had conversion surgery to THA. The mean Harris hip scores for the patients who did not have conversion surgery to THA improved from 53 to 88 points. Kaplan-Meier survival analysis showed no difference in the 11-year survival rate between patients with Stage II and Stage III disease (THA as an end point). However, the survival rate was lower for patients with Stage IV disease compared with patients with Stages II and III disease. The survival rate for patients in the steroid group was lower compared with the rates for patients in the idiopathic, alcoholic, trauma, and hyperlipidemia groups. At last followup, the stage of necrosis remained unchanged in 118 hips. CONCLUSIONS: We believe vascularized greater trochanter bone grafting is appropriate for young selected patients with mild to moderate collapse of the femoral head. LEVEL OF EVIDENCE: Level IV, therapeutic study. See Guidelines for Authors for a complete description of levels of evidence.