Bone Microdamage in Acute Knee Injury

Selvarajah, Logeswaran; Curtis, Anne M.; Kennedy, Oran D.

doi:10.1007/s11926-018-0791-8

Cited by 5 publications

(4 citation statements)

References 47 publications

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“…However, what is often observed as a direct result of joint injury, and in its immediate aftermath, is mechanical damage to the subchondral bone in the form of BMLs. These form as a direct result of injury and have been linked with pain and structural joint changes [ 10 , 11 , 12 , 13 ]. Later during disease development, abnormal bone remodeling modulates the local microenvironment further, but in a different way.…”

Section: Discussionmentioning

confidence: 99%

“…However, it is likely that they represent some kind of direct physical bone damage. Furthermore they have been linked with joint pain, and subsequent structural degradation of cartilage and other joint tissues [ 11 ]. Thus, it appears likely that direct mechanical damage to bone tissues [ 12 , 13 ], may indirectly affect cartilage tissue via bone–cartilage crosstalk.…”

Section: Introductionmentioning

confidence: 99%

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Impact of Fluid Flow Shear Stress on Osteoblast Differentiation and Cross-Talk with Articular Chondrocytes

Hinton¹,

Genoud

Early³

et al. 2022

IJMS

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Bone cells, in particular osteoblasts, are capable of communication with each other during bone growth and homeostasis. More recently it has become clear that they also communicate with other cell-types; including chondrocytes in articular cartilage. One way that this process is facilitated is by interstitial fluid movement within the pericellular and extracellular matrices. This stimulus is also an important mechanical signal in skeletal tissues, and is known to generate shear stresses at the micron-scale (known as fluid flow shear stresses (FFSS)). The primary aim of this study was to develop and characterize an in vitro bone–cartilage crosstalk system, to examine the effect of FFSS on these cell types. Specifically, we evaluated the response of osteoblasts and chondrocytes to FFSS and the effect of FFSS-induced soluble factors from the former, on the latter. This system will ultimately be used to help us understand the role of subchondral bone damage in articular cartilage degeneration. We also carried out a comparison of responses between cell lines and primary murine cells in this work. Our findings demonstrate that primary cells produce a more reliable and reproducible response to FFSS. Furthermore we found that at lower magnitudes , direct FFSS produces anabolic responses in both chondrocytes and osteoblasts, whereas higher levels produce more catabolic responses. Finally we show that exposure to osteoblast-derived factors in conditioned media experiments produced similarly catabolic changes in primary chondrocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Impact of Fluid Flow Shear Stress on Osteoblast Differentiation and Cross-Talk with Articular Chondrocytes

Hinton¹,

Genoud

Early³

et al. 2022

IJMS

Self Cite

View full text Add to dashboard Cite

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“…Inflammation is a hallmark of various pathological conditions such as those confined locally to the bone, including rheumatoid arthritis [28] and periodontitis [29]. Moreover, systemic inflammation is involved in a myriad of conditions such as kidney disease [30], inflammatory bowel disease [31], chronic skin inflammation [32], bacterial infection [33], cancer [34], acute injury [35], metabolic syndrome in obese patients [36], and diabetes [37]. Proinflammatory cytokines secreted in the bone vicinity enter blood circulation easily and travel to distant organs, causing systemic effects.…”

Section: Osteoclastogenic Cytokinesmentioning

confidence: 99%

Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption

Kitaura

Marahleh

Ohori

et al. 2020

IJMS

209

131

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The process of bone remodeling is the result of the regulated balance between bone cell populations, namely bone-forming osteoblasts, bone-resorbing osteoclasts, and the osteocyte, the mechanosensory cell type. Osteoclasts derived from the hematopoietic stem cell lineage are the principal cells involved in bone resorption. In osteolytic diseases such as rheumatoid arthritis, periodontitis, and osteoporosis, the balance is lost and changes in favor of bone resorption. Therefore, it is vital to elucidate the mechanisms of osteoclast formation and bone resorption. It has been reported that osteocytes express Receptor activator of nuclear factor κΒ ligand (RANKL), an essential factor for osteoclast formation. RANKL secreted by osteocytes is the most important factor for physiologically supported osteoclast formation in the developing skeleton and in pathological bone resorption such as experimental periodontal bone loss. TNF-α directly enhances RANKL expression in osteocytes and promotes osteoclast formation. Moreover, TNF-α enhances sclerostin expression in osteocytes, which also increases osteoclast formation. These findings suggest that osteocyte-related cytokines act directly to enhance osteoclast formation and bone resorption. In this review, we outline the most recent knowledge concerning bone resorption-related cytokines and discuss the osteocyte as the master regulator of bone resorption and effector in osteoclast formation.

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“…Available histological data associate the presence of a BML with microscopic tissue damage in cancellous bone, including microscopic cracks, diffuse damage, and trabecular microfracture. (11,15,20,24,42) These findings suggest that the presence of microscopic tissue damage in bone is required to replicate the majority of BMLs observed clinically. In humans, traumatic BMLs are often caused by impact loads such as a fall or associated with severe soft tissue damage (ie, ACL tears).…”

Section: Animal Models Of Bone Marrow Lesionsmentioning

confidence: 89%

Animal Models of Bone Marrow Lesions in Osteoarthritis

et al. 2022

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Bone marrow lesions are abnormalities in magnetic resonance images that have been associated with joint pain and osteoarthritis in clinical studies. Increases in the volume of bone marrow lesions have been associated with progression of joint degeneration, leading to the suggestion that bone marrow lesions may be an early indicator of-or even a contributor to-cartilage loss preceding irreversible damage to the joint. Despite evidence that bone marrow lesions play a role in osteoarthritis pathology, very little is known about the natural history of bone marrow lesions and their contribution to joint degeneration. As a result, there are limited data regarding the cell activity within a bone marrow lesion and any associated bone-cartilage cross-talk. Animal models provide the best approach for understanding bone marrow lesions at their early, reversible stages. Here, we review the few animal studies of bone marrow lesions. An ideal animal model of a bone marrow lesion occurs in joints large enough to accurately measure bone marrow lesion volume. Additionally, the ideal animal model would facilitate the study of bone-cartilage cross-talk by generating the bone marrow lesion immediately adjacent to subchondral bone and would do so without causing direct damage to neighboring soft tissues to isolate the effects of the bone marrow lesion on cartilage loss. Early reports demonstrate the feasibility of such an animal model. Given the irreversible nature of osteoarthritic changes in the joint, factors such as bone marrow lesions that are present early in disease pathogenesis remain an enticing target for new therapeutic approaches.

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Bone Microdamage in Acute Knee Injury

Cited by 5 publications

References 47 publications

Impact of Fluid Flow Shear Stress on Osteoblast Differentiation and Cross-Talk with Articular Chondrocytes

Impact of Fluid Flow Shear Stress on Osteoblast Differentiation and Cross-Talk with Articular Chondrocytes

Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption

Animal Models of Bone Marrow Lesions in Osteoarthritis

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