| Literature DB >> 32145378 |
Banu Bayram1, Afton K Limberg2, Christopher G Salib3, Jacob W Bettencourt4, William H Trousdale5, Eric A Lewallen6, Nicolas Reina7, Christopher R Paradise8, Roman Thaler9, Mark E Morrey10, Joaquin Sanchez-Sotelo11, Daniel J Berry12, Andre J van Wijnen13, Matthew P Abdel14.
Abstract
Arthrofibrosis is an abnormal histopathologic response, is debilitating for patients, and poses a substantial unsolved clinical challenge. This study characterizes molecular biomarkers and regulatory pathways associated with arthrofibrosis by comparing fibrotic and non-fibrotic human knee tissue. The fibrotic group encompasses 4 patients undergoing a revision total knee arthroplasty (TKA) for arthrofibrosis (RTKA-A) while the non-fibrotic group includes 4 patients undergoing primary TKA for osteoarthritis (PTKA) and 4 patients undergoing revision TKA for non-arthrofibrotic and non-infectious etiologies (RTKA-NA). RNA-sequencing of posterior capsule specimens revealed differences in gene expression between each patient group by hierarchical clustering, principal component analysis, and correlation analyses. Multiple differentially expressed genes (DEGs) were defined in RTKA-A versus PTKA patients (i.e., 2059 up-regulated and 1795 down-regulated genes) and RTKA-A versus RTKA-NA patients (i.e., 3255 up-regulated and 3683 down-regulated genes). Our findings define molecular and pathological markers of arthrofibrosis, as well as novel potential targets for risk profiling, early diagnosis and pharmacological treatment of patients.Entities:
Keywords: Acquired idiopathic stiffness; DEGs; Joint stiffness; RNA-seq; Total knee Arthroplasty
Mesh:
Year: 2020 PMID: 32145378 PMCID: PMC7217749 DOI: 10.1016/j.ygeno.2020.03.004
Source DB: PubMed Journal: Genomics ISSN: 0888-7543 Impact factor: 5.736