Project 461584
Curve progression, tissue remodelling and disease-modifying drugs in idiopathic scoliosis.
Curve progression, tissue remodelling and disease-modifying drugs in idiopathic scoliosis.
Project Information
| Study Type: | Unclear |
| Research Theme: | Biomedical |
Institution & Funding
| Principal Investigator(s): | Haglund, Lisbet A; Ouellet, Jean A |
| Co-Investigator(s): | Saran, Neil |
| Institution: | Research Institute of the McGill University Health Centre |
| CIHR Institute: | Musculoskeletal Health and Arthritis |
| Program: | |
| Peer Review Committee: | Biomedical Engineering |
| Competition Year: | 2022 |
| Term: | 5 yrs 0 mth |
Abstract Summary
Adolescent Idiopathic Scoliosis (AIS) is a curvature of the spine leading to a three-dimensional (3D) deformity, which affects 2-4% of children between 10-18 years of age. Clinically, patients with AIS are at risk that their spinal deformity progresses over time resulting in morbidities such as decreased pulmonary function and pain. Once severe, surgical management to straighten the spine is recommended. The overall goal of this proposal is to analyze the 3D deformity including load patterns, tissue homeostasis and pain with the overall aim to provide additional knowledge of the pathophysiology and clinical presentation of scoliosis. The open questions are; Can specific 3D parameters and curve patterns predict disease progression? Is there physiological evidence linking facet joint degeneration to posterior tethering leading to tissue remodelling and curve progression? Can senolytic and/or anti-inflammatory drugs reduce factors involved in tissue degeneration, tissue remodelling, and pain? Considering our previous findings that AIS patients have advanced facet cartilage degeneration, significantly more senescent cells than non-scoliotic cartilage and low bone density, we hypothesize that abnormal load contributes to an inflammatory environment driving both deformity and pain. A better understanding of these processes could lead to the identification of disease-modifying therapeutics targeting both progression and pain and simultaneously improve the effectiveness of bracing for AIS.
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