Background: The knee is one of the most frequently injured joints, including 80 000 anterior cruciate ligament (ACL) tears in the United States each year. Bone bruises are seen in over 80% of patients with ACL injuries, and have been associated with an overt loss of cartilage overlying those regions within 6 months of injury.
Hypothesis: The level of contact pressure developed in the human knee joint and the extent of articular cartilage and underlying subchondral bone injuries will depend on the mechanism of applied loads/moments during rupture of the ACL.
Study Design: Controlled laboratory study.
Methods: Seven knee pairs, flexed to 30 degrees , were loaded in compression or internal torsion until injury. Pressure-sensitive film recorded the magnitude and location of contact. Histologic analysis and magnetic resonance imaging were used to document microtrauma to the tibial plateau cartilage and subchondral bone.
Results: All specimens suffered ACL injury, either in the form of a midsubstance rupture or avulsion fracture. The contact area and pressures were higher for compression than torsion experiments. After being loaded, the articular cartilage in the central and posterior regions of the medial tibial plateau showed increased magnetic resonance imaging signal intensity, corresponding to an increased susceptibility to absorb water. Histologically, there were more microcracks in the subchondral bone and more articular cartilage damage in the compression than torsion experiments.
Conclusion: Significant damage occurs to the articular cartilage and underlying subchondral bone during rupture of the ACL. The types and extent of these tissue injuries are a function of the mechanism of ACL rupture.
Clinical Relevance: Patients suffering an ACL injury may be at risk of osteochondral damage, especially if the mechanism of injury involves a high compressive loading component, such as during a jump landing.
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http://dx.doi.org/10.1177/0363546508318046 | DOI Listing |
Pain
December 2024
Palo Alto Veterans Institute for Research, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, United States.
Previous preclinical and translational studies suggest that tissue trauma related to bony fracture and intervertebral disk disruption initiates the formation of pronociceptive antibodies that support chronic musculoskeletal pain conditions. This study tested this hypothesis in the monosodium iodoacetate (MIA) mouse model of osteoarthritis (OA) and extended the findings using OA patient samples. Monosodium iodoacetate was injected unilaterally into the knees of male and female wild-type (WT) and muMT mice (lacking B cells) to induce articular cartilage damage.
View Article and Find Full Text PDFInt J Rheum Dis
January 2025
Department of Orthopaedics, Shaanxi Rehbilitation Hospital, Xi'an, Shaanxi, China.
Background: Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.
View Article and Find Full Text PDFInt J Rheum Dis
January 2025
Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Disease, Minda Hospital of Hubei Minzu University, Enshi, China.
Osteoarthritis is a systemic disease that primarily damages articular cartilage and also affects the synovium, ligaments, and bone tissues. The key mechanisms involved are chondrocyte death and degradation of the extracellular matrix. This study aims to identify differentially expressed genes (DEGs) associated with ferroptosis and investigate their roles in the development of osteoarthritis.
View Article and Find Full Text PDFOsteoarthr Cartil Open
March 2025
Department of Regeneration Sciences and Engineering, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-Ku, Kyoto, 606-8507, Japan.
Objective: Osteoarthritis, a degenerative joint disease, requires innovative therapies due to the limited ability of cartilage to regenerate. Since mesenchymal stem cells (MSCs) provide a cell source for chondrogenic cells, we hypothesize that chemicals capable of enhancing the chondrogenic potential of MSCs with transforming growth factor-beta (TGFβ) in vitro may similarly promote chondrogenesis in articular cartilage in vivo.
Design: Chemical compounds that enhance the TGFβ signaling for chondrogenesis were investigated utilizing mesenchymal stem cells derived from human induced pluripotent stem cells.
Knee Surg Relat Res
January 2025
National Medical Research Radiological Center of the Ministry of Health of the Russian Federation, Koroleva st. 4, 249036, Obninsk, Russia.
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