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Molecular MRI in Rheumatoid Arthritis (RA)

Rheumatoid arthritis (RA) entails an autoimmune disorder involving chronic inflammation of joints. It leads to cartilage and bone degradation, resulting in a reduced quality of life due to chronic pain and musculoskeletal deficits (Jones et al. 5; Dakkak et al. 1). It affects approximately 1 percent of the population (Bhatnagar et al. 1; Wang et al. 3035). Molecular imaging is related to observing, detecting, and quantifying physiological and disease processes within an individual’s body at the molecular or cellular level (MacRitchie et al. 2). Imaging requires specific techniques or technologies to attain molecular imaging. Such instruments can act alone or combined with imaging agents to realize tissue status or detect biochemical markers, especially relating to a disease state. RA clinical imaging can be done through various methods like computed tomography, ultrasound, and magnetic resonance imaging (Xiao et al. 2; Wunder e al. 1341). Magnetic resonance imaging (MRI) is an excellent RA imaging technology as it has a better soft-tissue contrast and can offer details regarding inflammation within the joints (Bhatnagar et al. 1). In addition, it predicts the disease progression at an early stage.

MRI is essential in acquiring anatomic information, although it utilizes contrast imaging for molecular imaging due to its poor sensitivity. The MRI agents and biomarkers target synovial membrane inflammation during RA molecular imaging, the synovitis. Synovitis constitutes the upregulation of innate and adaptive immune cells along with fibroblast-like synoviocytes (Zheng et al., 824; Takeda and Sugimoto). Such immune response results in cartilage degradation and bone erosion (Hetta, Sharara, and Gouda 1043). The activated macrophages, T cells, and B cells found in synovial fluid are excellent molecular MRI imaging of RA targets (Jones et. 5). The MRI depends on the contrast agent choice when undertaking RA molecular imaging. T1-weighted MRI entails injecting paramagnetic metal agents. The most used agent is gadolinium-based as it curtails the T1 relaxation time leading to an improved signal. Gadolinium-based agent’s limited specificity and low sensitivity make T1-weighted MRI suboptimal for molecular imaging of RA. T2-weighted MRI usually constitutes injecting the superparamagnetic iron oxide nanoparticles (SPIONs). Such an act leads to improvement of negative contrast. Besides, SPIONs normally differ in size from ten to one hundred nm (Jones et al. 2). They are usually dextran-coated to elevate biocompatibility. Ultimately, active macrophage’s SPIONs intake at the inflammation site proves T2-weighted MRI as the best molecular imaging choice.

Another MRI biomarker is MR spectroscopy. It acquires different tissue metabolites’ molecular spectra to show data concerning the presence and concentration of various metabolites in the tissue. It offers more information than standard MRI, although its low sensitivity and poor spatial resolution limit its use as the agents of attention that occur in reduced concentrations (Jones et al. 2; Wilmot et al. 266). Besides, chemical exchange saturation transfer (CEST) is an MRI entailing magnetization exchange from the marked agent to the adjacent water or fluid molecules to view the signal decreased through the saturation consequence on water molecules only without viewing them on the target agent (Jones et al. 2). It depends on the target metabolite chemical composition and the radiofrequency initiating chemical exchange of the RA-infected portion. CEST MRI imaging directly relates to the portion transfer chemical exchange rate, enabling the molecular imaging of the particular metabolites identified at low concentrations. 19F MRI is another modality that allows direct fourine quantification of images, essential for evaluating the RA states or targeting efficiency. 19F compounds offer great attention due to their advantages, including being nontoxic and inert (Vu-Quang et al. 2MacRitchie et al. 5). Moreover, they can effectively be monitored.

RA appearance in MRI imaging can be based on synovitis. MRI images show proliferative synovitis as synovial membrane thickening. Such thickening indicates an intermediate to low signal intensity when the MRI used T1-weighted agents while T2-weighted agents showed high signal concentration. On the T1-weighted post-contrast images, the sore synovium reveals a fast advancement lasting almost five minutes after injection. There should be a delay between administering contrast and scanning as the capacity of synovitis enhancement surges at first before they are even out after four minutes. Images attained ten minutes after injecting contrast may be unsuccessful in delineating the synovitis range as gadolinium might diffuse into the synovial joint fluid (Sudoł-Szopińska, Jans and Teh 7). Such diffusion can distort the images of sore synovium. Using fat-suppressed gadolinium-enhanced T1-weighted images elevates the dissimilarity amongst T1 fat-saturated categorisations and sore synovium.

The synovial fluid on the MRI images demonstrates an amplified signal intensity on T2-weighted images. Furthermore, on the T1-weighted images, it is hypointense and indicates a reduced signal concentration on fat-suppressed gadolinium-enhanced MR images. MRI images are 2 to 3 dimensional (Put et al. 3). Using heavily T2-weighted images, synovitis can be easily identified as it has a reduced signal strength compared to joint effusion (Sudoł-Szopińska, Jans, and The 8). The images of tendon sheaths of inflamed synovium are similar to those in joint space synovitis. Therefore, MRI needs using FS T1-weighted MRI to explain the extent of the inflammatory variations in tendon sheaths more correctly. The subsequent images display synovial sheath thickening encompassing marked fat-suppressed gadolinium-enhanced TI-weighted images enhancement. MRI technique can also image bone marrow edema (BME) (Narvaez, abstract). BME predicts disease prognosis (Cimmino et al. 2). It is a hyperintense T2 signal zone in the trabecular bone (Sudoł-Szopińska, Jans and Teh 9). Given this information, an amplified signal intensity on T2-weighted images is seen as revealed by the synovial fluid on the MRI images.

Works Cited

Bhatnagar, Sumit, et al. “Oral and Subcutaneous Administration of a Near-Infrared Fluorescent Molecular Imaging Agent Detects Inflammation in A Mouse Model of Rheumatoid Arthritis.” Scientific Reports, vol. 9, no.1, 2019, pp. 1-11.

Cimmino, Marco A., et al. “Imaging in Arthritis: Quantifying Effects of Therapeutic Intervention Using MRI and Molecular Imaging.” Swiss Medical Weekly, vol. 141, no. 0102, 2012.

Dakkak, Y. J., et al. “What Is the Additional Value of MRI of the Foot to the Hand In Undifferentiated Arthritis to Predict Rheumatoid Arthritis Development?” Arthritis Research & Therapy, vol. 21, no.1, 2019, pp. 1-9.

Hetta, Waleed M., Sherin M. Sharara, and Gehan Ali Gouda. “Role of Magnetic Resonance Imaging and Ultrasonography in Diagnosis and Followup Rheumatoid Arthritis in Hand and Wrist Joints.” The Egyptian Journal of Radiology and Nuclear Medicine, vo. 49, no. 4, 2018, pp. 1043-1051.

MacRitchie, Neil, et al. “Molecular Imaging of Inflammation-Current and Emerging Technologies for Diagnosis and Treatment.” Pharmacology & Therapeutics, vo. 211, 2020, 107550.

Narvaez, José A., et al. “MR Imaging of Early Rheumatoid Arthritis.” Radiographics, vo. 30, no. 1, 2010, pp. 143-163.

Put, Stéphanie, et al. “Molecular Imaging of Rheumatoid Arthritis: Emerging Markers, Tools, and Techniques.” Arthritis Research & Therapy, vol. 16, no. 2, 2014, pp. 1-14.

Sudoł-Szopińska, Iwona, Lennart Jans, and James Teh. “Rheumatoid Arthritis: What do MRI and Ultrasound Show.” Journal of Ultrasonography, vol. 17, no. 68, 2017, 5.doi: 10.15557/JoU.2017.0001

Takeda, Akira, and Hideharu Sugimoto. “Growing Need for Diagnostic Precision in Rheumatoid Arthritis: Proposal of MR Imaging Criteria for Early Diagnosis.” Connective Tissue Disease-Current State of the Art. IntechOpen, 2020.

Vu-Quang, Hieu, et al. “Imaging Rheumatoid Arthritis in Mice Using Combined Near-Infrared and 19 F Magnetic Resonance Modalities.” Scientific Reports, vol. 9, no. 1, 2019, pp. 1-10.

Wang, Ming‑Yu, et al. “Diagnostic Value of High-Frequency Ultrasound and Magnetic Resonance Imaging in Early Rheumatoid Arthritis.” Experimental and Therapeutic Medicine, vol. 12, no. 5, 2016, pp. 3035-3040. doi: 10.3892/etm.2016.3695

Wilmot, Andrew, et al. “Molecular Imaging: An Innovative Force in Musculoskeletal Radiology.” American Journal of Roentgenology, vol. 201, no. 2, 2013, pp. 264-277. doi:10.2214/AJR.13.10713

Wunder, A., et al. “Molecular Imaging: Novel Tools in Visualizing Rheumatoid Arthritis.” Rheumatology, vol. 44, no. 11, 2005, pp. 1341-1349.

Xiao, Shuyi, et al. “In Vivo Nano Contrast-enhanced Photoacoustic Imaging for Dynamically Lightening the Molecular Changes of Rheumatoid Arthritis.” Materials & Design, 2021,

Zheng, Fang, et al. “Molecular Imaging with Macrophage Crig-Targeting Nanobodies for Early and Preclinical Diagnosis in a Mouse Model of Rheumatoid Arthritis.” Journal of Nuclear Medicine, vol. 55, no. 5, 2014, pp. 824-829. doi: 10.2967/jnumed.113.130617


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