Bone marrow lesions in the knee: the clinical conundrum

Bassiouni, Hassan

doi:10.1111/j.1756-185x.2010.01539.x

Cited by 9 publications

(6 citation statements)

References 35 publications

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“…The spatial association of these changes strongly supports the notion of a close functional relationship between subchondral bone and articular cartilage. This relationship is further highlighted by examining bone marrow lesions (BMLs), discrete abnormalities that can be visualized in the subchondral bone using magnetic resonance imaging (MRI; reviewed in Bassiouni, 90 and Daheshia and Yao 91 ). Although commonly observed in symptomatic OA, 92–95 BMLs are also seen in early (pre-radiographic or asymptomatic) OA.…”

Section: Enhanced Crosstalk Associated With Bmlsmentioning

confidence: 99%

Bone–cartilage crosstalk: a conversation for understanding osteoarthritis

2016

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Although cartilage degradation is the characteristic feature of osteoarthritis (OA), it is now recognized that the whole joint is involved in the progression of OA. In particular, the interaction (crosstalk) between cartilage and subchondral bone is thought to be a central feature of this process. The interface between articular cartilage and bone of articulating long bones is a unique zone, which comprises articular cartilage, below which is the calcified cartilage sitting on and intercalated into the subchondral bone plate. Below the subchondral plate is the trabecular bone at the end of the respective long bones. In OA, there are well-described progressive destructive changes in the articular cartilage, which parallel characteristic changes in the underlying bone. This review examines the evidence that biochemical and biomechanical signaling between these tissue compartments is important in OA disease progression and asks whether such signaling might provide possibilities for therapeutic intervention to halt or slow disease development.

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Section: Enhanced Crosstalk Associated With Bmlsmentioning

confidence: 99%

Bone–cartilage crosstalk: a conversation for understanding osteoarthritis

2016

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“…An increased trabecular number, decreased trabecular spacing, and reduced hardness of the bone in OA [ 22 ], due to decreased mineralization [ 23 ], characterize the subchondral bone, especially in zones underlying cartilage degeneration. Discrete zones of subchondral bone that can be imaged using magnetic resonance (MR), termed bone marrow lesions (BML), are frequently observed in both established OA and in early OA, but rarely in symptom free individuals [ 24 , 25 ]. BMLs arise in regions of predicted high loading and contain abnormal bone, with areas of osteocyte death, areas of bone sclerosis with reduced mineral density [ 26 ].…”

Section: Osteoblasts In Oamentioning

confidence: 99%

Osteoblast-Chondrocyte Interactions in Osteoarthritis

Findlay

Atkins

2014

Curr Osteoporos Rep

130

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There is now general agreement that osteoarthritis (OA) involves all structures in the affected joint, culminating in the degradation of the articular cartilage. It is appropriate to focus particularly on the subchondral bone because characteristic changes occur in this tissue with disease progression, either in parallel, or contributing to, the loss of cartilage volume and quality. Changes in both the articular cartilage and the subchondral bone are mediated by the cells in these two compartments, chondrocytes and cells of the osteoblast lineage, respectively, whose primary roles are to maintain the integrity and function of these tissues. In addition, altered rates of bone remodeling across the disease process are due to increased or decreased osteoclastic bone resorption. In the altered mechanical and biochemical environment of a progressively diseased joint, the cells function differently and show a different profile of gene expression, suggesting direct effects of these external influences. There is also ex vivo and in vitro evidence of chemical crosstalk between the cells in cartilage and subchondral bone, suggesting an interdependence of events in the two compartments and therefore indirect effects of, for example, altered loading of the joint. It is ultimately these cellular changes that explain the altered morphology of the cartilage and subchondral bone. With respect to crosstalk between the cells in cartilage and bone, there is evidence that small molecules can transit between these tissues. For larger molecules, such as inflammatory mediators, this is an intriguing possibility but remains to be demonstrated. The cellular changes during the progression of OA almost certainly need to be considered in a temporal and spatial manner, since it is important when and where observations are made in either human disease or animal models of OA. Until recently, comparisons have been made with the assumption, for example, that the subchondral bone is behaviorally uniform, but this is not the case in OA, where regional differences of the bone are evident using magnetic resonance imaging (MRI). Nevertheless, an appreciation of the altered cell function during the progression of OA will identify new disease modifying targets. If, indeed, the cartilage and subchondral bone behave as an interconnected functional unit, normalization of cell behavior in one compartment may have benefits in both tissues.

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“…The loss of the articular cartilage changes the stresses on the underlying subchondral bone, which itself has pain receptors. Subchondral bone may react to increasing shearing forces by becoming reactive and sclerotic [23]. Bone scintigraphy studies have shown an increase in delayed phase tracer in the tibiofemoral compartment in of patients reporting knee pain [24].…”

Section: Aetiologymentioning

confidence: 99%