18F-FPRGD2 PET/CT imaging of musculoskeletal disorders

Withofs, Nadia; Charlier, Émilie; Simoni, Paolo; Alvarez-Miezentseva, Victoria; Mievis, Frédéric; Giacomelli, Fabrice; Mella, Christine; Gambhir, Sanjiv S.; Malaise, Olivier; Seny, Dominique de; Malaise, Michel; Hustinx, Roland

doi:10.1007/s12149-015-1011-5

Cited by 11 publications

(18 citation statements)

References 51 publications

(78 reference statements)

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“…A similar apoptosis, related to signal loss with the matrix, has been described in other systems, such as in epithelial cells, and was called anoikis [117]. Our laboratory found that integrin α V , β 3 , and β 5 were upregulated during OA chondrocyte dedifferentiation [118]. The α V β 3 complex was also upregulated at the surface of dedifferentiated OA chondrocytes, compared to freshly-isolated OA chondrocytes [118].…”

Section: Apoptosis In Chondrocytes and Osteoarthritis (Oa) Developmentioning

confidence: 77%

“…Our laboratory found that integrin α V , β 3 , and β 5 were upregulated during OA chondrocyte dedifferentiation [118]. The α V β 3 complex was also upregulated at the surface of dedifferentiated OA chondrocytes, compared to freshly-isolated OA chondrocytes [118]. Differential integrin expression status might be crucial in sensitizing chondrocytes to cell death induced by the ECM component.…”

Section: Apoptosis In Chondrocytes and Osteoarthritis (Oa) Developmentioning

confidence: 99%

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Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

Charlier

Relić

Deroyer

et al. 2016

IJMS

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259

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Osteoarthritis (OA) is a joint pathology characterized by progressive cartilage degradation. Medical care is mainly based on alleviating pain symptoms. Compelling studies report the presence of empty lacunae and hypocellularity in cartilage with aging and OA progression, suggesting that chondrocyte cell death occurs and participates to OA development. However, the relative contribution of apoptosis per se in OA pathogenesis appears complex to evaluate. Indeed, depending on technical approaches, OA stages, cartilage layers, animal models, as well as in vivo or in vitro experiments, the percentage of apoptosis and cell death types can vary. Apoptosis, chondroptosis, necrosis, and autophagic cell death are described in this review. The question of cell death causality in OA progression is also addressed, as well as the molecular pathways leading to cell death in response to the following inducers: Fas, Interleukin-1β (IL-1β), Tumor Necrosis factor-α (TNF-α), leptin, nitric oxide (NO) donors, and mechanical stresses. Furthermore, the protective role of autophagy in chondrocytes is highlighted, as well as its decline during OA progression, enhancing chondrocyte cell death; the transition being mainly controlled by HIF-1α/HIF-2α imbalance. Finally, we have considered whether interfering in chondrocyte apoptosis or promoting autophagy could constitute therapeutic strategies to impede OA progression.

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Section: Apoptosis In Chondrocytes and Osteoarthritis (Oa) Developmentioning

confidence: 77%

Section: Apoptosis In Chondrocytes and Osteoarthritis (Oa) Developmentioning

confidence: 99%

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

Charlier

Relić

Deroyer

et al. 2016

IJMS

Self Cite

259

220

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“…The selection of a RGD‐based tracer was guided by previous medical studies conducted in our Institution and by the experience acquired in Fluorine‐18 derivatives . The routine [ 18 F]FPRGD 2 production is time‐consuming and tedious; it involves a multistep radiochemical sequence, among which 1 step releases volatile radioactive compounds.…”

Section: Resultsmentioning

confidence: 99%

“NOTA‐PRGD₂ and NODAGA‐PRGD₂: Bioconjugation, characterization, radiolabelling, and design space”

Salvé

Avohou

Monbaliu

et al. 2018

Labelled Comp Radiopharmac

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This work reports on the development of amide bond bioconjugation for the production of -NOTA and -NODAGA PRGD using batch strategy and microfluidic reactor technology. The final radiolabelling step was fully optimized using Design of Experiments and Design Space approaches, hence targeting robust labelling yields in routine. Optimal labelling conditions were defined in sodium acetate buffer as 168 μg/mL peptide concentration, 4.9 pH, 47.5°C temperature, and 12.5-minute reaction time. Upon optimization, the Gallium-68 radiolabelling was fully automated. All the work was designed to be compliant to the GMP environment and to support the pharmaceutical scale-up.

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“…In addition, [ 18 F]FPRGD 2 uptake was also observed in glenohumeral, left hip, and right ankle joints ((a) blue arrows) as well as in the left total knee arthroplasty ((a) orange arrow). The observation of [ 18 F]FPRGD 2 uptake in musculoskeletal disorders has already been published [ 6 ].…”

Section: Figurementioning

confidence: 99%

A First Report on [¹⁸F]FPRGD₂ PET/CT Imaging in Multiple Myeloma

Withofs

Cousin

Prijck

et al. 2017

Contrast Media & Molecular Imaging

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An observational study was set up to assess the feasibility of [18F]FPRGD2 PET/CT for imaging patients with multiple myeloma (MM) and to compare its detection rate with low dose CT alone and combined [18F]NaF/[18F]FDG PET/CT images. Four patients (2 newly diagnosed patients and 2 with relapsed MM) were included and underwent whole-body PET/CT after injection of [18F]FPRGD2. The obtained images were compared with results of low dose CT and already available results of a combined [18F]NaF/[18F]FDG PET/CT. In total, 81 focal lesions (FLs) were detected with PET/CT and an underlying bone destruction or fracture was seen in 72 (89%) or 8 (10%) FLs, respectively. Fewer FLs (54%) were detected by [18F]FPRGD2 PET/CT compared to low dose CT (98%) or [18F]NaF/[18F]FDG PET/CT (70%) and all FLs detected with [18F]FPRGD2 PET were associated with an underlying bone lesion. In one newly diagnosed patient, more [18F]FPRGD2 positive lesions were seen than [18F]NaF/[18F]FDG positive lesions. This study suggests that [18F]FPRGD2 PET/CT might be less useful for the detection of myeloma lesions in patients with advanced disease as all FLs with [18F]FPRGD2 uptake were already detected with CT alone.

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18F-FPRGD2 PET/CT imaging of musculoskeletal disorders

Abstract: The ¹⁸F-FPRGD₂ uptake in joints, spine degenerative diseases and tendons was highly prevalent in our population. Up to one-third of ¹⁸F-FPRGD₂ foci showed no FDG uptake suggesting that ¹⁸F-FPRGD₂ signal may not be related to inflammatory angiogenesis only.

Cited by 11 publications

References 51 publications

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

“NOTA‐PRGD₂ and NODAGA‐PRGD₂: Bioconjugation, characterization, radiolabelling, and design space”

A First Report on [¹⁸F]FPRGD₂ PET/CT Imaging in Multiple Myeloma

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18F-FPRGD2 PET/CT imaging of musculoskeletal disorders

Abstract: The ¹⁸F-FPRGD₂ uptake in joints, spine degenerative diseases and tendons was highly prevalent in our population. Up to one-third of ¹⁸F-FPRGD₂ foci showed no FDG uptake suggesting that ¹⁸F-FPRGD₂ signal may not be related to inflammatory angiogenesis only.

Cited by 11 publications

References 51 publications

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

“NOTA‐PRGD2 and NODAGA‐PRGD2: Bioconjugation, characterization, radiolabelling, and design space”

A First Report on [18F]FPRGD2 PET/CT Imaging in Multiple Myeloma

Contact Info

Product

Resources

About

“NOTA‐PRGD₂ and NODAGA‐PRGD₂: Bioconjugation, characterization, radiolabelling, and design space”

A First Report on [¹⁸F]FPRGD₂ PET/CT Imaging in Multiple Myeloma