Is Osteoarthritis a Vascular Disease?
Osteoarthritis (OA) is now considered as a multifaceted disease affecting various articular tissues, including cartilage, bone, synovium, and surrounding ligaments. The pathophysiology strongly implicates intricate chemical communication, primarily through cytokines, leading to the production of deg...
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| Format: | Article |
| Language: | English |
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IMR Press
2024-03-01
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| Series: | Frontiers in Bioscience-Landmark |
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| Online Access: | https://www.imrpress.com/journal/FBL/29/3/10.31083/j.fbl2903113 |
| _version_ | 1797238654910857216 |
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| author | Jon Olansen Jonathan P. Dyke Roy K. Aaron |
| author_facet | Jon Olansen Jonathan P. Dyke Roy K. Aaron |
| author_sort | Jon Olansen |
| collection | DOAJ |
| description | Osteoarthritis (OA) is now considered as a multifaceted disease affecting various articular tissues, including cartilage, bone, synovium, and surrounding ligaments. The pathophysiology strongly implicates intricate chemical communication, primarily through cytokines, leading to the production of degradative enzymes in cartilage, inflammatory peptides in synovium, and structural changes in bone, resulting in characteristic clinical features such as joint deformities and loss of cartilage space seen on X-rays. Recent studies highlight the previously underestimated role of subchondral bone in OA, revealing its permeability to cytokines and raising questions about the influence of abnormal perfusion on OA pathophysiology, suggesting a vascular component in the disease’s etiology. In essence, alterations in bone perfusion, including reduced venous outflow and intraosseous hypertension, play a crucial role in influencing the physicochemical environment of subchondral bone, impacting osteoblast cytokine expression and contributing to trabecular remodeling, changes in chondrocyte phenotype, and ultimately cartilage matrix degeneration in OA. Dynamic contrast (gadolinium) enhanced magnetic resonance imaging (DCE-MRI) was used to quantify perfusion kinetics in normal and osteoarthritic subchondral bone, demonstrating that decreased perfusion temporally precedes and spatially correlates with cartilage lesions in both young Dunkin-Hartley (D-H) guinea pigs and humans with osteoarthritis. Pharmacokinetic analysis of DCE-MRI generated data reveals decreased tracer clearance and outflow obstruction in the medial tibial plateau of osteoarthritic guinea pigs, coinciding with progressive cartilage degradation, loss of Safranin O staining, and increased expression of matrix metalloproteinases and interleukin-1. Positron emission tomographic (PET) scanning using 18F-Fluoride reveals a relationship among bone blood flow, cartilage lesions, and 18F-Fluoride influx rate in OA, highlighting the intricate relationships between decreased perfusion, altered bone metabolism, and the progression of osteoarthritis. These findings, supported by 18F-Fluoride PET data, suggest the presence of venous stasis associated with outflow obstruction, emphasizing the role of decreased subchondral bone perfusion in the pathophysiology of OA and its association with reduced osteoblast activity and advanced cartilage degeneration. |
| first_indexed | 2024-04-24T17:39:05Z |
| format | Article |
| id | doaj.art-f673925e8d894d6dab4751f4077a59b8 |
| institution | Directory Open Access Journal |
| issn | 2768-6701 |
| language | English |
| last_indexed | 2024-04-24T17:39:05Z |
| publishDate | 2024-03-01 |
| publisher | IMR Press |
| record_format | Article |
| series | Frontiers in Bioscience-Landmark |
| spelling | doaj.art-f673925e8d894d6dab4751f4077a59b82024-03-28T02:27:55ZengIMR PressFrontiers in Bioscience-Landmark2768-67012024-03-0129311310.31083/j.fbl2903113S2768-6701(24)01243-7Is Osteoarthritis a Vascular Disease?Jon Olansen0Jonathan P. Dyke1Roy K. Aaron2Department of Orthopedic Surgery, Warren Alpert Medical School of Brown University, Providence, RI 02903, USACitigroup Biomedical Imaging Center, Weill Cornell Medical Center, New York, NY 10021, USADepartment of Orthopedic Surgery, Warren Alpert Medical School of Brown University, Providence, RI 02903, USAOsteoarthritis (OA) is now considered as a multifaceted disease affecting various articular tissues, including cartilage, bone, synovium, and surrounding ligaments. The pathophysiology strongly implicates intricate chemical communication, primarily through cytokines, leading to the production of degradative enzymes in cartilage, inflammatory peptides in synovium, and structural changes in bone, resulting in characteristic clinical features such as joint deformities and loss of cartilage space seen on X-rays. Recent studies highlight the previously underestimated role of subchondral bone in OA, revealing its permeability to cytokines and raising questions about the influence of abnormal perfusion on OA pathophysiology, suggesting a vascular component in the disease’s etiology. In essence, alterations in bone perfusion, including reduced venous outflow and intraosseous hypertension, play a crucial role in influencing the physicochemical environment of subchondral bone, impacting osteoblast cytokine expression and contributing to trabecular remodeling, changes in chondrocyte phenotype, and ultimately cartilage matrix degeneration in OA. Dynamic contrast (gadolinium) enhanced magnetic resonance imaging (DCE-MRI) was used to quantify perfusion kinetics in normal and osteoarthritic subchondral bone, demonstrating that decreased perfusion temporally precedes and spatially correlates with cartilage lesions in both young Dunkin-Hartley (D-H) guinea pigs and humans with osteoarthritis. Pharmacokinetic analysis of DCE-MRI generated data reveals decreased tracer clearance and outflow obstruction in the medial tibial plateau of osteoarthritic guinea pigs, coinciding with progressive cartilage degradation, loss of Safranin O staining, and increased expression of matrix metalloproteinases and interleukin-1. Positron emission tomographic (PET) scanning using 18F-Fluoride reveals a relationship among bone blood flow, cartilage lesions, and 18F-Fluoride influx rate in OA, highlighting the intricate relationships between decreased perfusion, altered bone metabolism, and the progression of osteoarthritis. These findings, supported by 18F-Fluoride PET data, suggest the presence of venous stasis associated with outflow obstruction, emphasizing the role of decreased subchondral bone perfusion in the pathophysiology of OA and its association with reduced osteoblast activity and advanced cartilage degeneration.https://www.imrpress.com/journal/FBL/29/3/10.31083/j.fbl2903113osteoarthritisvenous stasiscytokinescartilage degradationsubchondral boneperfusion |
| spellingShingle | Jon Olansen Jonathan P. Dyke Roy K. Aaron Is Osteoarthritis a Vascular Disease? Frontiers in Bioscience-Landmark osteoarthritis venous stasis cytokines cartilage degradation subchondral bone perfusion |
| title | Is Osteoarthritis a Vascular Disease? |
| title_full | Is Osteoarthritis a Vascular Disease? |
| title_fullStr | Is Osteoarthritis a Vascular Disease? |
| title_full_unstemmed | Is Osteoarthritis a Vascular Disease? |
| title_short | Is Osteoarthritis a Vascular Disease? |
| title_sort | is osteoarthritis a vascular disease |
| topic | osteoarthritis venous stasis cytokines cartilage degradation subchondral bone perfusion |
| url | https://www.imrpress.com/journal/FBL/29/3/10.31083/j.fbl2903113 |
| work_keys_str_mv | AT jonolansen isosteoarthritisavasculardisease AT jonathanpdyke isosteoarthritisavasculardisease AT roykaaron isosteoarthritisavasculardisease |