Arthrofibrosis following total knee arthroplasty (TKA) is a debilitating condition typically diagnosed based on clinical findings. To gain insight into the histopathologic immune cell microenvironment of arthrofibrosis, we assessed the extent of tissue fibrosis and quantified immune cell populations in specific tissue regions of the posterior capsule. We investigated specimens from three prospectively-collected, matched cohorts, grouped as patients receiving a primary TKA for osteoarthritis, revision TKA for arthrofibrosis, and revision TKA for non-arthrofibrotic, non-infectious reasons. Specimens were evaluated using hematoxylin and eosin staining, picrosirius red staining, immunofluorescence, and immunohistochemistry with Aperio®-based digital image analysis. Increased collagen deposition and increased number of α-SMA/ACTA2 expressing myofibroblasts were present in the arthrofibrosis group compared to the two non-arthrofibrotic groups. CD163 + macrophages were the most abundant immune cell type in any capsular sample with specific enrichment in the synovial tissue. CD163 + macrophages were significantly decreased in the fibrotic tissue region of arthrofibrosis patients compared to the patients with primary TKA, and significantly increased in adipose tissue region of arthrofibrotic specimens compared to non-arthrofibrotic specimens. Synovial CD117 + mast cells were significantly decreased in arthrofibrotic adipose tissue. Together, these findings inform diagnostic and targeted therapeutic strategies by providing insight into the underlying pathogenetic mechanisms of arthrofibrosis.
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http://dx.doi.org/10.1038/s41598-022-22175-3 | DOI Listing |
ACS Nano
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Department of Gynecology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, P. R. China.
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January 2025
Stomatological Hospital, School of Stomatology, Southern Medical University, Guangzhou, Guangdong 510280, China. E-mail:
Severe combined immunodeficiency disease (SCID), characterized by profound immune system dysfunction, can lead to life-threatening infections and death. Animal models play a pivotal role in elucidating biological processes and advancing therapeutic strategies. Recent advances in gene-editing technologies, including zinc-finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), CRISPR/Cas9, and base editing, have significantly enhanced the generation of SCID models.
View Article and Find Full Text PDFZool Res
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School of Basic Medicine, Institute of Brain Science and Disease, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Brain Diseases, Qingdao University, Qingdao, Shandong, 266071, China. E-mail:
Iron is the most abundant transition metal in the brain and is essential for brain development and neuronal function; however, its abnormal accumulation is also implicated in various neurological disorders. The olfactory bulb (OB), an early target in neurodegenerative diseases, acts as a gateway for environmental toxins and contains diverse neuronal populations with distinct roles. This study explored the cell-specific vulnerability to iron in the OB using a mouse model of intranasal administration of ferric ammonium citrate (FAC).
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