Core decompression versus other joint preserving treatments for osteonecrosis of the femoral head: a meta-analysis

Sadile, Francesco; Bernasconi, Alessio; Russo, Sergio; Maffulli, Nicola

doi:10.1093/bmb/ldw010

Cited by 96 publications

(65 citation statements)

References 37 publications

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“…Long-term use of highdose glucocorticoids is the most common cause of NOFH, and it occurs mostly in young adults [30]. At present, the clinical treatment of NOFH includes conservative treatment (biophysical stimulation such as pulsed electromagnetic field) and surgical methods (such as core decompression), but the effect is not significant [31]. In addition, most patients undergo one or more artificial joint revision operations, which imposes serious economic and mental burdens on society and patients' families [32].…”

Section: Discussionmentioning

confidence: 99%

MiR-596 inhibits osteoblastic differentiation and cell proliferation by targeting Smad3 in steroid-induced osteonecrosis of femoral head

Liu

Lei

2020

J Orthop Surg Res

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Background: It is reported that miR-596 has a potential diagnostic value for non-traumatic osteonecrosis of the femoral head (NOFH), but its underlying mechanisms in NOFH is unclear. Methods: The expression of miR-596 and Smad3 was detected by western blot and quantitative real-time PCR. The relationship between the two molecules was explored using Dual-Luciferase Reporter Assay. Glucocorticoid (GC)dexamethasone, was used to induce bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation, and the effects of miR-596 on BMSC osteogenic differentiation and proliferation were determined.Results: MiR-596 expression was upregulated, while Smad3 expression was inhibited in the bone marrow samples of patients with steroid-induced osteonecrosis of femoral head (SANFH). Overexpression of miR-596 inhibited the proliferation and osteogenic differentiation of BMSCs induced by GC. Meanwhile, the opposite results were observed in the miR-596 inhibitor group. In addition, Smad3 was a target gene of miR-596, and negatively regulated by miR-596. The promotion effect of the miR-596 inhibitor on BMSC proliferation and osteogenic differentiation was reversed by si-Smad3.Conclusion: MiR-596 can suppress GC-BMSC osteoblastic differentiation and proliferation by regulating Smad3 expression.

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Section: Discussionmentioning

confidence: 99%

MiR-596 inhibits osteoblastic differentiation and cell proliferation by targeting Smad3 in steroid-induced osteonecrosis of femoral head

Liu

Lei

2020

J Orthop Surg Res

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“…were able to prove that especially classic core decompression does not improve clinical outcomes compared with other jointpreserving therapies. There even is some indication for less beneficial overall results [45]. On the whole, determining the role of core decompression remains difficult since lots of modifications have been described so far, and there is a lack of comparing studies.…”

Section: Discussionmentioning

confidence: 99%

Results of advanced core decompression in patients with osteonecrosis of the femoral head depending on age and sex—a prospective cohort study

et al. 2020

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Background: Core decompression is a common surgical technique to treat osteonecrosis of the femoral head. The aim of this study is to evaluate the effect of the parameters "age" and "sex" on the outcome of this type of treatment. Methods: A prospective cohort study was performed. Eighty-six osteonecrotic hips with a mean follow-up of 32.5 months (± 24.8) after advanced core decompression were analysed regarding age-and sex-dependent treatment failure. Additionally, the modified Harris Hip Score and Numeric Rating Scale were compared regarding the parameters age and sex. Results: The mean hip survival of the male participants was 51.3 months (39.4% treatment failure), whereas females presented a longer, thus not significant, mean survival of 61.4 months (30% therapy failure; p = 0.48). The further evaluation revealed significantly better survival in the patients aged < 40 years (mean survival 66.09 months, 16% treatment failure) in comparison to those aged ≥ 40 years (mean survival 50.14 months, 46% therapy failure; p = 0.03). The modified Harris Hip Score and Numeric Rating Scale results of patients whose treatment did not fail during the study period were similar, irrespective of the patient's sex or age. Conclusions: The study shows that the number of therapy failures is significantly higher in older patients, with 40 years of age marking the borderline. Patients' sex does not seem to affect the outcome of treatment, and postoperative clinical scores appear to be identical with individuals not affected by therapy failure. Since age and sex are unalterable parameters, the study helps to provide valuable predictions regarding the chances of long-term hip survival after treatment of osteonecrosis.

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“…Historically, in adults with primary ON of weight bearing joints, the most common treatments include invasive forms of secondary and tertiary prevention, including core decompression [51] with or without stem cell infusion [52], vascularized fibular graft [53], and ultimately total joint replacement [54]. Hence, new diagnoses of ON, initially made by the radiologist and confirmed by the orthopedic or dental surgeon or clinician [55], rarely undergo a rigorous workup for thrombophilia or hypofibrinolysis [5].…”

Section: Discussionmentioning

confidence: 99%

Case report: primary osteonecrosis associated with thrombophilia-hypofibrinolysis and worsened by testosterone therapy

et al. 2017

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BackgroundFamilial and acquired thrombophilia are often etiologic for idiopathic hip and jaw osteonecrosis (ON), and testosterone therapy (TT) can interact with thrombophilia, worsening ON.Case presentationCase 1: A 62-year-old Caucasian male (previous deep venous thrombosis), on warfarin 1 year for atrial fibrillation (AF), had non-specific right hip-abdominal pain for 2 years. CT scan revealed bilateral femoral head ON without collapse. Coagulation studies revealed Factor V Leiden (FVL) heterozygosity, 4G/4G plasminogen activator inhibitor (PAI) homozygosity, high anti-cardiolipin (ACLA) IgM antibodies, and endothelial nitric oxide (NO) synthase (eNOS) T786C homozygosity (reduced conversion of L-arginine to NO, required for bone health). Apixaban 5 mg twice daily was substituted for warfarin; and L-arginine 9 g/day was started to increase NO. On Apixaban for 8 months, he became asymptomatic. Case 2: A 32-year-old hypogonadal Caucasian male had 10 years of unexplained tooth loss, progressing to primary jaw ON with cavitation 8 months after starting TT gel 50 mg/day. Coagulation studies revealed FVL heterozygosity, PAI 4G/4G homozygosity, and the lupus anticoagulant. TT was discontinued. Jaw pain was sharply reduced within 2 months.ConclusionsIdiopathic ON, often caused by thrombophilia-hypofibrinolysis, is worsened by TT, and its progression may be slowed or stopped by discontinuation of TT and, thereafter, anticoagulation. Recognition of thrombophilia-hypofibrinolysis before joint collapse facilitates anticoagulation which may stop ON, preserving joints.

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Core decompression versus other joint preserving treatments for osteonecrosis of the femoral head: a meta-analysis

Abstract: Further studies are needed to identify the best therapeutic approach to the ONFH.

Cited by 96 publications

References 37 publications

MiR-596 inhibits osteoblastic differentiation and cell proliferation by targeting Smad3 in steroid-induced osteonecrosis of femoral head

MiR-596 inhibits osteoblastic differentiation and cell proliferation by targeting Smad3 in steroid-induced osteonecrosis of femoral head

Results of advanced core decompression in patients with osteonecrosis of the femoral head depending on age and sex—a prospective cohort study

Case report: primary osteonecrosis associated with thrombophilia-hypofibrinolysis and worsened by testosterone therapy

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