circSSPO boosts growth of esophageal squamous cell carcinoma through upregulation of micrRNA-6820-5p-mediated KLK8 and PKD1 expression.

Investigation on a competitive endogenous RNA (ceRNA) network attracted lots of attention due its function in cancer regulation. Here, we probed into the possible molecular mechanism of circSSPO/microRNA-6820-5p (miR-6820-5p)/kallikrein-related peptidase 8 (KLK8)/PKD1 network in the esophageal squamous cell carcinoma (ESCC). Following whole-transcriptome sequencing and differential analysis in collected ESCC tissue samples, circRNA-miRNA-mRNA regulatory network affecting ESCC was investigated. After interaction measurement among circSSPO/miR-6820-5p/KLK8/PKD1, their regulatory roles in ESCC cell functions in vitro and xenograft tumor growth and lung metastasis in vivo were analyzed. The bioinformatics prediction and sequencing results screened that circSSPO, miR-6820-5p, KLK8, and PKD1 were associated with ESCC development. In ESCC, miR-6820-5p was expressed at very low levels, while circSSPO, KLK8, and PKD1 were highly expressed. In vitro cell experiments further proved that circSSPO competitively inhibited miR-6820-5p to induce ESCC cell malignant properties. Moreover, knockdown of KLK8 or PKD1 inhibited ESCC cell malignant properties. circSSPO also promoted the tumorigenic and metastasis of ESCC through the upregulation of KLK8 and PKD1 expression in vivo. We found that circSSPO was an oncogenic circRNA that was significantly abundant in ESCC tissues and circSSPO exhibited an oncogenic activity in ESCC by elevating expression of KLK8 and PKD1 through suppressing miR-6820-5p expression.

Corrigendum: Single-cell RNA sequencing reveals the difference in human normal and degenerative nucleus pulposus tissue profiles and cellular interactions.

[This corrects the article DOI: 10.3389/fcell.2022.910626.].

Single-cell RNA landscape of osteoimmune microenvironment in osteoporotic vertebral compression fracture and Kümmell's disease.

Background: Single-cell RNA sequencing (scRNA-seq) enables specific analysis of cell populations at single-cell resolution; however, there is still a lack of single-cell-level studies to characterize the dynamic and complex interactions between osteoporotic vertebral compression fractures (OVCFs) and Kümmell's disease (KD) in the osteoimmune microenvironment. In this study, we used scRNA-seq analysis to investigate the osteoimmune microenvironment and cellular composition in OVCFs and KD. Methods: ScRNA-seq was used to perform analysis of fractured vertebral bone tissues from one OVCF and one KD patients, and a total of 8,741 single cells were captured for single-cell transcriptomic analysis. The cellularity of human vertebral bone tissue was further analyzed using uniform manifold approximation and projection. Pseudo-time analysis and gene enrichment analysis revealed the biological function of cell fate and its counterparts. CellphoneDB was used to identify the interactions between bone cells and immune cells in the osteoimmune microenvironment of human vertebral bone tissue and their potential functions. Results: A cellular profile of the osteoimmune microenvironment of human vertebral bone tissue was established, including mesenchymal stem cells (MSCs), pericytes, myofibroblasts, fibroblasts, chondrocytes, endothelial cells (ECs), granulocytes, monocytes, T cells, B cells, plasma cells, mast cells, and early erythrocytes. MSCs play an immunoregulatory function and mediate osteogenic differentiation and cell proliferation. The differentiation trajectory of osteoclasts in human vertebral bone tissue was also revealed. In addition, ECs actively participate in inflammatory infiltration and coupling with bone cells. T and B cells actively participate in regulating bone homeostasis. Finally, by identifying the interaction of ligand-receptor pairs, we found that immune cells and osteoclasts have bidirectional regulatory characteristics, have the effects of regulating bone resorption by osteoclasts and promoting bone formation, and are essential for bone homeostasis. It is also highlighted that CD8-TEM cells and osteoclasts might crosstalk via CD160-TNFRSF14 ligand-receptor interaction. Conclusion: Our analysis reveals a differential landscape of molecular pathways, population composition, and cell-cell interactions during OVCF development into KD. OVCFs exhibit a higher osteogenic differentiation capacity, owing to abundant immune cells. Conversely, KD results in greater bone resorption than bone formation due to depletion of MSCs and a relatively suppressed immune system, and this immune imbalance eventually leads to vertebral avascular necrosis. The site of action between immune cells and osteoclasts is expected to be a new therapeutic target, and these results may accelerate mechanistic and functional studies of osteoimmune cell types and specific gene action in vertebral avascular necrosis and pathological bone loss diseases, paving the way for drug discovery.

Long non-coding RNA ERVK13-1 aggravates osteosarcoma through the involvement of microRNA-873-5p/KLF5 axis.

OBJECTIVE: To explore the effect and mechanism of long noncoding RNA ERVK13-1 on osteosarcoma (OS) cell development by regulation of miR-873-5p/KLF5 axis. METHODS: The expression of ERVK13-1 in the collected tissue was detected by RT-qPCR, and then the relationship between ERVK13-1 expression and clinical characteristics of OS patients was analyzed. After OS cell lines were transfected with miR-873-5p inhibitor, si-ERVK13-1, si-KLF5 or their negative controls, the expression of ERVK13-1, miR-873-5p, and KLF5 in OS cell lines were measured, followed by determination of their effects on cell proliferation, migration, and invasion abilities. Moreover, the binding relationships of ERVK13-1 and miR-873-5p, as well as miR-873-5p and KLF5, were verified by the dual-luciferase reporter gene assay. RESULTS: Highly expressed ERVK13-1 was found in OS tissues, which was closely related to tumor size, tumor node metastasis, and distant metastasis. The overall survival of OS patients with high expression of ERVK13-1 was poorer than those with low expression of ERVK13-1. Elevated ERVK13-1 and KLF5 but suppressed miR-873-5p was observed in the OS cell lines U2OS and MG63. Transfection with miR-873-5p inhibitor enhanced the malignant potentials of OS cells, and transfection with si-ERVK13-1 or si-KLF5 reduced these abilities of OS cells. ERVK13-1 bound to miR-873-5p and KLF5 was a target gene of miR-873-5p. CONCLUSION: The ERVK13-1/miR-873-5p/KLF5 axis confers vital effect on the occurrence and progression of OS, thus providing possible guidance for the clinical treatment of OS.

Corrigendum: Single-cell RNA sequencing reveals the difference in human normal and degenerative nucleus pulposus tissue profiles and cellular interactions.

[This corrects the article DOI: 10.3389/fcell.2022.910626.].

FBP1 knockdown decreases ovarian cancer formation and cisplatin resistance through EZH2-mediated H3K27me3.

Worldwide, ovarian cancer (OC) is the seventh common cancer and the second most common cause of cancer death in women. Due to high rates of relapse, there is an urgent need for the identification of new targets for OC treatment. The far-upstream element binding protein 1 (FBP1) and enhancer of zeste homolog 2 (EZH2) are emerging proto-oncogenes that regulate cell proliferation and metastasis. In the present study, Oncomine data analysis demonstrated that FBP1 was closely associated with the development of OC, and The Cancer Genome Atlas (TCGA) data analysis indicated that there was a positive correlation between FBP1 and EZH2 in ovarian tissues. Moreover, we found that FBP1 knockdown suppressed tumor formation in nude mice and cisplatin resistance of OC cells, but the role of FBP1 in the cisplatin resistance of OC cells remained unclear. In addition, we verified physical binding between FBP1 and EZH2 in OC cells, and we demonstrated that FBP1 knockdown enhanced cisplatin cytotoxicity in OC cells and down-regulated EZH2 expression and trimethylation of H3K27. These results suggested that FBP1 increases cisplatin resistance of OC cells by up-regulating EZH2/H3K27me3. Thus, FBP1 is a prospective novel target for the development of OC treatment.

Single-Cell RNA Sequencing Reveals the Difference in Human Normal and Degenerative Nucleus Pulposus Tissue Profiles and Cellular Interactions.

Background: The nucleus pulposus is a constituent structure of the human intervertebral disc, and its degeneration can cause intervertebral disc degeneration (IDD). However, the cellular and molecular mechanisms involved remain elusive. Methods: Through bioinformatics analysis, the single-cell transcriptome sequencing expression profiles of human normal nucleus pulposus (NNP) cells and human degenerative nucleus pulposus (DNP) cells were compared to clarify the transcriptome differential expression profiles of human NNP and DNP. The single-cell sequencing results of the two samples were analyzed using bioinformatics methods to compare the differences in histiocytosis between human NNP and DNP, map the histiocytes of NNP and DNP, perform cell differentiation trajectories for the cell populations of interest and predict cell function, and explore their heterogeneity by pathway analysis and Gene Ontology analysis. Results: Nine cell types were identified, which were chondrocyte 1, chondrocyte 2, chondrocyte 3, chondrocyte 4, chondrocyte 5, endothelial, macrophage, neutrophil, and T cells. Analysis of the proportion of chondrocytes in different tissues revealed that chondrocyte 1 accounted for a higher proportion of NNP cells and highly expressed COL2A1 compared with DNP cells; chondrocyte 2, chondrocyte 3, chondrocyte 4, and chondrocyte 5 accounted for a higher proportion of DNP cells compared with NNP cells. Among them, chondrocyte 2 was an inhibitory calcified chondrocyte with high expression of MGP, chondrocytes 3 were fibrochondrocytes with high expression of COL1A1, chondrocytes 4 were chondrocytes that highly express pain inflammatory genes such as PTGES, and chondrocytes 5 were calcified chondrocytes with high expression of FN1 (chondrocytes 4 and chondrocytes 5 were found for the first time in a study of single-cell transcriptome sequencing of disc tissue). Cell trajectory analysis revealed that chondrocyte 1 was at the beginning of the trajectory and chondrocyte 3 was at the end of the trajectory, while chondrocyte 5 appeared first in the trajectory relative to chondrocyte 2 and chondrocyte 4. Conclusion: After functional identification of the specifically expressed genes in five chondrocytes, it was found that chondrocyte 1 was a chondrocyte with high expression of COL2A1, COL9A2, COL11A2, and CHRDL2 in a high proportion of NNP cells, and chondrocyte 3 was a fibrochondrocyte with high expression of COL1A1, COL6A3, COL1A2, COL3A1, AQP1, and COL15A1 in an increased proportion during nucleus pulposus cell degeneration. Through cell trajectory analysis, it was found that chondrocytes 5 specifically expressing FN1, SESN2, and GDF15 may be the key cells leading to degeneration of nucleus pulposus cells. Chondrocytes 2 expressing MGP, MT1G, and GPX3 may play a role in reversing calcification and degeneration, and chondrocytes 4 expressing PTGES, TREM1, and TIMP1 may play a role in disc degeneration pain and inflammation.

Involvement of the TNF-α/SATB2 axis in the induced apoptosis and inhibited autophagy of osteoblasts by the antipsychotic Risperidone.

BACKGROUND: Risperidone, an atypical antipsychotic, impedes serotonin and dopamine receptor systems. Meanwhile, tumor necrosis factor-α (TNF-α) is known to participate in regulating osteoblast functions. Consequently, the current study aimed to investigate whether the influences of Risperidone on osteoblast functions are associated with TNF-α and special AT-rich sequence-binding protein (SATB2). METHODS: Firstly, we searched the DGIdb, MEM and GeneCards databases to identify the critical factors involved in the effects of Risperidone on osteoblasts, as well as their interactions. Afterwards, osteoblast cell line MC3T3-E1 was transduced with lentivirus carrying si-TNF-α, si-SATB2 or both and subsequently treated with Risperidone. Various abilities including differentiation, autophagy and apoptosis of osteoblasts were examined after different treatments. Finally, animal experiments were performed with Risperidone alone or together with lentivirus to verify the function of Risperidone in vivo and the mechanism. RESULTS: It was found that Risperidone might promote TNF-α expression, thereby inhibiting the expression of SATB2 to affect the autophagy and apoptosis in osteoblasts. Furthermore, as shown by our experimental findings, Risperidone treatment inhibited the differentiation and autophagy, and promoted the apoptosis of osteoblasts, as evidenced by elevated levels of OPG, p62, cleaved PARP1, cleaved caspase-3, cleaved caspase-8, and cleaved caspase-9, and reduced levels of LC3 II/I, Beclin1, collagen I, and RANKL. In addition, Risperidone was also found to elevate the expression of TNF-α to down-regulate SATB2, thereby inhibiting the differentiation and autophagy and enhancing the apoptosis of osteoblasts in vitro and in vivo. CONCLUSIONS: Collectively, our findings indicated that Risperidone affects the differentiation of osteoblasts by inhibiting autophagy and enhancing apoptosis via TNF-α-mediated down-regulation of SATB2.

Expression of Matrix Metalloprotein 13 in Injury Model of Articular Chondrocyte in Rabbits and Analysis of Nano-Drug-Loading System.

This study aimed to analyze the application of a responsive nano-drug-loading system in injury model of articular chondrocyte in rabbits, as well as its effect on expression of matrix metalloprotein 13 (MMP13). The nanoprecipitation method was adopted to prepare camptothecin (CPT)-loaded poly ethylene glycol (PEG)-Poly caprolactone (PCL) and PEG-PCL nanoparticles without CPT. Afterward, the above mentioned nano-drug-loaded system was used to treat an in vitro scratch model of articular chondrocytes. According to different treatment plans, they were divided into groups: G0 (administered CPT-PEG-PCL nanomedicine), G1 (administered PEG-PCL drug), G2 (saline control), and G3 (healthy control). Results showed that the drug-loading capacity and efficiency of CPT-PEG-PCL was higher than that of PEG-PCL. The levels of type II collagen and hyaluronic acid in G0 was higher than that in G1 and G2. The levels of type II collagen and hyaluronic acid in G0 were not obviously different from those in G3. The level of MMP13 in G0 was lower than that in G1 and G2 and the level of tissue inhibitor of metalloproteinases 1 (TIMP1) in G0 was higher than that in G1 and G2. The proliferation activity of cells in G0 was higher than that in G1 and G2, but there was no obvious difference when compared with G3. In conclusion, CPT-PEG-PCL has stronger long-term circulation capacity and drug-loading efficiency. It can effectively up-regulate the levels of type II collagen, hyaluronic acid, and TIMP1, as well as reduce the synthesis and secretion of MMP13 and promote the repair of articular cartilage damage.

miR-129-3p alleviates chondrocyte apoptosis in knee joint fracture-induced osteoarthritis through CPEB1.

BACKGROUND: Osteoarthritis (OA), a refractory disease, is one of the leading contributors for disability worldwide. Since chondrocyte is the only resident cell in cartilage, this study aims to explore the roles of miR-129-3p and CPEB1 in chondrocyte apoptosis in knee joint fracture-induced OA. METHODS: Cartilage was collected from 20 OA patients who underwent total knee replacement (OA group) and 20 patients with knee contusion (normal group). Then, miR-129-3p and CPEB1 levels in the cartilage were quantified by qRT-PCR. Primary rat chondrocytes in the knee were isolated and identified by toluidine blue staining and immunofluorescent staining of type II collagen. OA cellular models were induced by TNF-α treatment, in which miR-129-3p and CPEB1 expressions were assessed. Subsequently, cell viability, apoptosis, and the expression levels of apoptotic protein and caspase-3 were measured. Dual luciferase reporter assay identified the interaction between miR-129-3p and CPEB1. RESULTS: Patients in the OA group had decreased miR-129-3p expression and increased CPEB1 expression than those in the normal group. TNF-α treatment successfully induced the OA cellular model. Downregulated miR-129-3p and upregulated CPEB1 expressions were found in OA-treated chondrocytes. miR-129-3p overexpression or CPEB1 knockdown improved chondrocyte viability and attenuated apoptosis, and vice versa. miR-129-3p negatively regulated CPEB1, thus ameliorating apoptosis and enhancing cell viability. CONCLUSION: miR-129-3p negatively targeted CPEB1 to facilitate chondrocyte viability and hamper apoptosis.

[Mid-term effectiveness of Coflex interspinous dynamic internal fixation combined with spinal fusion for lumbar disc degeneration].

Objective: To evaluate the effectiveness of Coflex interspinous dynamic internal fixation combined with spinal fusion for lumbar disc degeneration. Methods: The clinical data of 39 patients with two-level lumbar disc degeneration who met the selection criteria between June 2010 and December 2011 was retrospectively analyzed. They were divided into group A (20 cases, simple lumbar decompression and fusion) and group B (19 cases, Coflex interspinous dynamic internal fixation combined with spinal fusion) according to different surgical methods. There was no significant difference in age, gender, disease diagnosis, lesion segment, disease duration, Oswestry disability index (ODI), visual analogue scale (VAS) score, and the intervertebral height, foramen intervertebral height (FIH), and range of motion (ROM) of upper operative segment and adjacent segment between the two groups ( P>0.05). ODI and VAS score were used to evaluate the effectiveness before operation and at last follow-up, and the improvement rates were calculated. The intervertebral height [anterior disc height (ADH), middle disc height (MDH), and posterior disc height (PDH)], FIH, and ROM were measured and compared between the two groups. Results: The operation time and intraoperative blood loss in group A were significantly more than those in group B ( P<0.05), and there was no significant difference in hospitalization time between the two groups ( t=0.992, P=0.328). All patients were followed up; the follow-up time was 33-50 months (mean, 40.5 months) in group A and 39-51 months (mean, 42.6 months) in group B. No complication such as displacement, loosening, or rupture of internal fixator was found in both groups. At last follow-up, ODI and VAS score of the two groups significantly improved when compared with preoperative scores ( P<0.05). At last follow-up, there was no significant difference in ODI, VAS score, and improvement rate of ODI between the two groups ( P>0.05); the improvement rate of VAS score in group B was significantly higher than that in group A ( t=2.245, P=0.031). There was no significant difference in the intervertebral height and FIH of the upper operative segment at last follow-up between the two groups and between preoperation and last follow-up in the two groups ( P>0.05). At last follow-up, the ADH of adjacent segment in group B was significantly higher than that in group A, and MDH, PDH, and FIH were significantly lower than those in group A ( P<0.05). Compared with preoperation, the ADH of adjacent segment in group A decreased and MDH, PDH, and FIH increased at last follow-up ( P<0.05), while all indexes in group B did not change significantly ( P>0.05). The ROM of adjacent segment in group A increased significantly at last follow-up ( t=2.318, P=0.026). There was significant difference in ROM of adjacent segment between the two groups ( P<0.05). Conclusion: The mid-term effectiveness of Coflex interspinous dynamic internal fixation combined with spinal fusion is similar to that of simple decompression fusion. For those patients whose adjacent segments of the responsible segments have degeneration but have no symptoms or mild symptoms, this treatment can slow down the adjacent segment degeneration.

Risk factors for osteoporosis in liver cirrhosis patients measured by transient elastography.

Osteoporosis or osteopenia is a common complication in patients with cirrhosis, but little is known about the risk factors for the occurrence of osteoporosis.Patients with liver cirrhosis due to chronic virus infection and alcoholic abuse were enrolled. Bone mineral density (BMD) was determined using dual-energy x-ray absorptiometry (DXA). Osteoporosis was diagnosed according to WHO criteria. The severity of liver stiffness was measured by Fibroscan. Demographic data, such as age, gender, weight, height, and body mass index (BMI), were collected. Logistic regression analysis was used to recognize the risk factors of osteoporosis in patients with cirrhosis.A total of 446 patients were included in this study: 217 had liver cirrhosis (male, 74.2%; mean age, 57.2 ±â€Š10.27) and 229 were matched controls (male, 69%, mean age, 56.69 ±â€Š9.37). Osteoporosis was found in 44 patients (44/217, 20.3%). The spine and hip BMD in cirrhotic patients were significantly lower than that in controls. When the cirrhotic and control subjects were stratified by age, gender, and BMI, the significant difference was also observed in women patients, patients older than 60, and patients with BMI < 18. Multivariate analysis showed that the older age [odds ratio (OR) = 1.78, P = .046], lower BMI (OR = 0.63, P = .049), greater fibroscan score (OR = 1.15, P = .009), and liver cirrhosis induced by alcohol liver disease (OR = 3.42, P < .001) were independently associated with osteoporosis in cirrhotic patients.Osteoporosis occurred in about one-fifth of patients with liver cirrhosis, which was associated with age, BMI, Fibroscan score, and alcohol liver disease related liver cirrhosis.

Leptocarpin Suppresses Proliferation, Migration, and Invasion of Human Osteosarcoma by Targeting Type-1 Insulin-Like Growth Factor Receptor (IGF-1R).

BACKGROUND Leptocarpin (LTC) has drawn much attention for suppressing tumor growth or reducing inflammation. However, the effect of LTC on osteosarcoma has rarely been reported. Our object was to determine whether LTC suppresses MG63 cell proliferation, migration, and invasion, and whether type-1 insulin-like growth factor receptor (IGF-1R) is one of the targets in LTC suppressing osteosarcoma. MATERIAL AND METHODS Cytotoxicity of LTC was performed by use of a cell-counting kit-8 (CCK-8). RNA interference (RNAi) or pEABE-bleo IGF-1R plasmid were used for silencing or overexpressing IGF-1R, Western blot (WB) analysis was used for IGF-1R expression, CCK-8 for proliferation, and transwell assay for migration and invasion. RESULTS LTC (23.533 µM) treatment for 48 h was taken as the 50% inhibiting concentration (IC50), which significantly (P<0.05) suppressed MG63 cells proliferation, migration, and invasion. LTC (IC50) obviously inhibited IGF-1R expression in MG63 cells, with similar effect to small interfering RNA (siRNA), while pEABE-bleo IGF-1R transfection overexpressed IGF-1R. siRNA silencing IGF-1R suppressed MG63 cells proliferation, migration, and invasion, while pEABE-bleo IGF-1R transfection was significantly (P<0.05) promoted. With or without siRNA or pEABE-bleo IGF-1R transfection, LTC (IC50) suppressed MG63 cells proliferation, migration, and invasion. The effect of LTC (IC50) combined with siRNA on suppressing MG63 cells proliferation, migration, and invasion was more obvious, while the effect of LTC (IC50) combined with pEABE-bleo IGF-1R transfection was less significant (P<0.05). CONCLUSIONS LTC suppressed osteosarcoma proliferation, migration, and invasion by inhibiting IGF-1R expression. IGF-1R is one of the targets in LTC suppressing osteosarcoma.

Limited Unilateral Decompression and Pedicle Screw Fixation with Fusion for Lumbar Spinal Stenosis with Unilateral Radiculopathy: A Retrospective Analysis of 25 Cases.

OBJECTIVE: Lumbar spinal stenosis is conventionally treated with surgical decompression. However, bilateral decompression and laminectomy is more invasive and may not be necessary for lumbar stenosis patients with unilateral radiculopathy. We aimed to report the outcomes of unilateral laminectomy and bilateral pedicle screw fixation with fusion for patients with lumbar spinal stenosis and unilateral radiculopathy. METHODS: Patients with lumbar spinal stenosis with unilateral lower extremity radiculopathy who received limited unilateral decompression and bilateral pedicle screw fixation were included and evaluated using visual analog scale (VAS) pain and the Oswestry Disability Index (ODI) scores preoperatively and at follow-up visits. Ligamentum flavum thickness of the involved segments was measured on axial magnetic resonance images. RESULTS: Twenty-five patients were included. The mean preoperative VAS score was 6.6±1.6 and 4.6±3.1 for leg and back pain, respectively. Ligamentum flavum thickness was comparable between the symptomatic and asymptomatic side (p=0.554). The mean follow-up duration was 29.2 months. The pain in the symptomatic side lower extremity (VAS score, 1.32±1.2) and the back (VAS score, 1.75±1.73) significantly improved (p=0.000 vs. baseline for both). The ODI improved significantly postoperatively (6.60±6.5; p=0.000 vs. baseline). Significant improvement in VAS pain and ODI scores were observed in patients receiving single or multi-segment decompression fusion with fixation (p<0.01). CONCLUSION: Limited laminectomy and unilateral spinal decompression followed by bilateral pedicle screw fixation with fusion achieves satisfactory outcomes in patients with spinal stenosis and unilateral radiculopathy. This procedure is less damaging to structures that are important for maintaining posterior stability of the spine.

Effect of Osteonecrosis Intervention Rod Versus Core Decompression Using Multiple Small Drill Holes on Early Stages of Necrosis of the Femoral Head: A Prospective Study on a Series of 60 Patients with a Minimum 1-Year-Follow-Up.

INTRODUCTION: The conventional CD used 10 mm drill holes associated with a lack of structural support. Thus, alternative methods such as a tantalum implant, small drill holes, and biological treatment were developed to prevent deterioration of the joint. The treatment of CD by multiple 3.2 mm drill holes could reduce the femoral neck fracture and partial weight bearing was allowed. This study was aimed to evaluate the effect of osteonecrosis intervention rod versus core decompression using multiple small drill holes on early stages of necrosis of the femoral head. METHOD: From January 2011 to January 2012, 60 patients undergoing surgery for osteonecrosis with core decompression were randomly assigned into 2 groups based on the type of core decompression used: (1) a total of 30 osteonecrosis patients (with 16 hips on Steinburg stageⅠ,20 hips on Steinburg stageⅡ) were treated with a porous tantalum rod insertion. The diameter of the drill hole for the intervention rod was 10mm.(2) a total of 30 osteonecrosis patients (with 14 hips on Steinburg stageⅠ,20 hips on Steinburg stageⅡ) were treated with core decompression using five drill holes on the lateral femur, the diameter of the hole was 3.2 mm. The average age of the patient was 32.6 years (20-45 years) and the average time of follow-up was 25.6 months (12- 28 months) in the rod implanted group. The average age of the patient was 35.2 years (22- 43 years) and the average time of follow-up was 26.3 months (12-28 months) in the small drill holes group. RESULTS: The average of surgical time was 40 min, and the mean volume of blood loss was 30 ml in both surgical groups. The average of Harris score was improved from 56.2 ± 7.1 preoperative to 80.2 ± 11.4 at the last follow-up in the rod implanted group (p < 0.05). The mean Harris score was improved from 53.8 ± 6.6 preoperative to 79.7 ± 13.2 at the last follow-up in the small drill holes group (p<0. 05). No significant difference was observed in Harris score between the two groups. At the last follow-up, 28 of 36 hips were at the same radiographic stages as pre-operation, and 8 deteriorated in the rod implanted group. 26 of 34 hips were at the same radiographic stage as pre-operation, and 8 deteriorated in the small drill holes group. No significant difference was observed in radiographic stage between the two groups. There was no favourable result on the outcome of a tantalum intervention implant compared to multiple small drill holes. DISCUSSION: CD via multiple small drill holes would allow similar postoperative load-bearing and seems to result in similar or even better clinical outcome without the prolonged implantation of an expensive tantalum implant. A tantalum rod intervention and core decompression using multiple small drill holes were effective on the stage I hips rather than stage II hips.