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Objective: The risks of nonunion and subsidence are high in patients with bone density loss undergoing spinal fusion surgery. The internal application of recombinant human bone morphogenic protein 2 (rhBMP-2) in an interbody cage improves spinal fusion; however, related complications have been reported. Denosumab, a human monoclonal antibody targeting the receptor activator of nuclear factor kappa B ligand (RANKL), hinders osteoblast differentiation and function. Therefore, this study aimed to observe the combined effect of the local application of rhBMP-2 in a lumbar cage and systemic RANKL inhibition on postoperative spinal fusion in patients with bone density loss undergoing posterior lumbar interbody fusion (PLIF).
Methods: This retrospective observational study included 251 consecutive patients with spinal stenosis who underwent PLIF at a single center between 2017 and 2021. Clinical outcomes were assessed, and radiographic evaluations included lumbar flexion, extension, range of motion, and subsidence. Statistical analyses were conducted to identify the combined effect of the treatment and the subsidence and spinal fusion status.
Results: One hundred patients were included in the final analysis. Denosumab treatment significantly reduced the rate of osteolysis (p = 0.013). When denosumab was administered in combination with rhBMP-2, the fusion status remained similar; however, the incidences of postoperative osteolysis and postoperative oozing day decreased.
Conclusion: The combined use of rhBMP-2 and RANKL inhibition in patients with bone density loss can enhance bone formation after PLIF with fewer complications than rhBMP-2 alone.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762388 | PMC |
http://dx.doi.org/10.14245/ns.2346702.351 | DOI Listing |
Cytometry B Clin Cytom
September 2025
School of Medical Sciences, Universidade Estadual de Campinas (Unicamp), Campinas, Brazil.
Acute promyelocytic leukemia (APL) is a medical emergency that needs immediate diagnosis and treatment. Podoplanin, a transmembrane glycoprotein that binds CLEC-2 on platelets, was recently demonstrated to be abnormally expressed in leukemic blasts in APL, as opposed to other forms of AML, in a study using thawed primary cells. This study aimed to explore and validate the diagnostic accuracy of measuring podoplanin expression by flow cytometry in the differential diagnosis of APL and other forms of acute myeloid leukemia (AML) as part of the diagnostic work-up of all cases suspected of AML in an academic hematology center.
View Article and Find Full Text PDFRev Med Liege
September 2025
Service de Pneumologie, CHU de Liège, Belgique.
Obstructive sleep apnea-hypopnea syndrome (OSAHS) is an underrated and heavy public health problem. Polysomnography (PSG) remains GOLD-standard examination but we also use ambulatory screening tests including Brizzy, which measures mandibular movements. The aim is to report on our experience with the Brizzy and compare it with PSG data.
View Article and Find Full Text PDFJ Intern Med
September 2025
Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy.
Adv Healthc Mater
September 2025
Epigenetics Research Laboratory, Institute of Nano Science and Technology, Knowledge City, Sector 81, Mohali, Punjab, 140306, India.
Acute Myeloid Leukemia (AML) is a heterogeneous hematological malignancy with an altered bone marrow microenvironment sheltering leukemic stem cells (LSCs). LSCs are characterized as self-renewing and highly proliferative cancer stem cells and accumulate abnormal genetic and epigenetic factors contributing to their uncontrolled proliferation. Chromosomal translocation t(9;11)(p22;q23) forms fusion oncoprotein, MLL-AF9, and regulates the transcription factor, C-Myb, which is highly expressed in AML.
View Article and Find Full Text PDFMol Ther
September 2025
Department of Medicine, UMass Chan Medical School, Worcester, MA, USA; Department of Genetic and Cellular Medicine, UMass Chan Medical School, Worcester, MA, USA; Horae Gene Therapy Center, UMass Chan Medical School, Worcester, MA, USA; Li Weibo Institute for Rare Diseases Research, UMass Chan Medic
The interleukin (IL)-1 pathway is a key mediator of inflammation and innate immune responses. Its dysregulation contributes to rheumatoid arthritis (RA) and autoinflammatory diseases (AIDs). In this study, we develop a recombinant adeno-associated virus (rAAV)-based gene therapy to deliver an inflammation-inducible, secreted human IL-1 receptor antagonist (sIL-1Ra) as a complementary approach to existing IL-1 blockers.
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