Subchondral Bone

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Henning Madry - One of the best experts on this subject based on the ideXlab platform.

  • The Osteochondral Unit: The Importance of the Underlying Subchondral Bone
    Cartilage Restoration, 2018
    Co-Authors: Tamás Oláh, Henning Madry
    Abstract:

    The term osteochondral unit reflects the tight functional association of the articular cartilage, calcified cartilage, and the Subchondral Bone. Due to its special composition of collagen type II, aggrecan, and water, the extracellular matrix of the articular cartilage provides exceptional tensile strength and compressive resilience to the tissue. A radiologically denser, discrete band of mineralized cartilage, the tidemark separates the articular cartilage from the calcified cartilage. The hydroxyapatite-containing calcified cartilage forms an undulating transitional zone, attaching the cartilage to the Subchondral Bone. The Subchondral Bone plays a key role in mechanically and metabolically supporting the articular cartilage, maintaining the joint shape, and absorbing shock. It consists of two regions: the Subchondral Bone plate is a dense bony lamella which merges into a network of trabecular Bone called the subarticular spongiosa. The cavities of the Subchondral Bone contain blood vessels which are important sources of nutrients and signaling molecules for the deeper layers of cartilage. Several diseases affect the osteochondral unit. The most well-known of them is osteoarthritis (OA), a disease of the entire joint including the cartilage, Subchondral Bone, and other structures. Avascular necrosis and osteochondritis dissecans are diseases primarily affecting the Subchondral Bone, often leading to OA and focal cartilage defects. In these diseases and during the repair of osteochondral defects, phenomena like Subchondral Bone cysts, Bone marrow edema, and intralesional osteophytes are common findings in both patients and translational animal models. Currently all “cartilage restoration” strategies now recognize the importance of considering the entire osteochondral unit during implementation, to avoid chondral deterioration or even delamination.

  • A novel algorithm for a precise analysis of Subchondral Bone alterations.
    Scientific Reports, 2016
    Co-Authors: Patrick Orth, Magali Cucchiarini, Lars Goebel, Henning Madry
    Abstract:

    Subchondral Bone alterations are emerging as considerable clinical problems associated with articular cartilage repair. Their analysis exposes a pattern of variable changes, including intra-lesional osteophytes, residual microfracture holes, peri-hole Bone resorption, and Subchondral Bone cysts. A precise distinction between them is becoming increasingly important. Here, we present a tailored algorithm based on continuous data to analyse Subchondral Bone changes using micro-CT images, allowing for a clear definition of each entity. We evaluated this algorithm using data sets originating from two large animal models of osteochondral repair. Intra-lesional osteophytes were detected in 3 of 10 defects in the minipig and in 4 of 5 defects in the sheep model. Peri-hole Bone resorption was found in 22 of 30 microfracture holes in the minipig and in 17 of 30 microfracture holes in the sheep model. Subchondral Bone cysts appeared in 1 microfracture hole in the minipig and in 5 microfracture holes in the sheep model (n = 30 holes each). Calculation of inter-rater agreement (90% agreement) and Cohen’s kappa (kappa = 0.874) revealed that the novel algorithm is highly reliable, reproducible, and valid. Comparison analysis with the best existing semi-quantitative evaluation method was also performed, supporting the enhanced precision of this algorithm.

  • alterations of the Subchondral Bone in osteochondral repair translational data and clinical evidence
    European Cells & Materials, 2013
    Co-Authors: Patrick Orth, Magali Cucchiarini, Dieter Kohn, Henning Madry
    Abstract:

    Alterations of the Subchondral Bone are pathological features associated with spontaneous osteochondral repair and with articular cartilage repair procedures. The aim of this review is to discuss their incidence, extent and relevance, focusing on recent knowledge gained from both translational models and clinical studies of articular cartilage repair. Efforts to unravel the complexity of Subchondral Bone alterations have identified (1) the upward migration of the Subchondral Bone plate, (2) the formation of intralesional osteophytes, (3) the appearance of Subchondral Bone cysts, and (4) the impairment of the osseous microarchitecture as potential problems. Their incidence and extent varies among the different small and large animal models of cartilage repair, operative principles, and over time. When placed in the context of recent clinical investigations, these deteriorations of the Subchondral Bone likely are an additional, previously underestimated factor that influences the long-term outcome of cartilage repair strategies. Understanding the role of the Subchondral Bone in both experimental and clinical articular cartilage repair thus holds great promise of being translated into further improved cell- or biomaterial-based techniques to preserve and restore the entire osteochondral unit.

  • temporal and spatial migration pattern of the Subchondral Bone plate in a rabbit osteochondral defect model
    Osteoarthritis and Cartilage, 2012
    Co-Authors: Patrick Orth, Stefan Graber, Magali Cucchiarini, Gunter Kaul, Dieter Kohn, Henning Madry
    Abstract:

    Summary Objective Upward migration of the Subchondral Bone plate is associated with osteochondral repair. The aim of this study was to quantitatively monitor the sequence of Subchondral Bone plate advancement in a lapine model of spontaneous osteochondral repair over a 1-year period and to correlate these findings with articular cartilage repair. Design Standardized cylindrical osteochondral defects were created in the rabbit trochlear groove. Subchondral Bone reconstitution patterns were identified at five time points. Migration of the Subchondral Bone plate and areas occupied by osseous repair tissue were determined by histomorphometrical analysis. Tidemark formation and overall cartilage repair were correlated with the histomorphometrical parameters of the Subchondral Bone. Results The Subchondral Bone reconstitution pattern was cylindrical at 3 weeks, infundibuliform at 6 weeks, plane at 4 and 6 months, and hypertrophic after 1 year. At this late time point, the osteochondral junction advanced 0.19 [95% confidence intervals (CI) 0.10–0.30] mm above its original level. Overall articular cartilage repair was significantly improved by 4 and 6 months but degraded after 1 year. Subchondral Bone plate migration correlated with tidemark formation ( r  = 0.47; P r  = 0.11; P  > 0.44). Conclusions The Subchondral Bone plate is reconstituted in a distinct chronological order. The lack of correlation suggests that articular cartilage repair and Subchondral Bone reconstitution proceed at a different pace and that the advancement of the Subchondral Bone plate is not responsible for the diminished articular cartilage repair in this model.

  • The basic science of the Subchondral Bone
    Knee Surgery Sports Traumatology Arthroscopy, 2010
    Co-Authors: Henning Madry, C. Niek Van Dijk, Magdalena Mueller-gerbl
    Abstract:

    In the past decades, considerable efforts have been made to propose experimental and clinical treatments for articular cartilage defects. Yet, the problem of cartilage defects extending deep in the underlying Subchondral Bone has not received adequate attention. A profound understanding of the basic anatomic aspects of this particular site, together with the pathophysiology of diseases affecting the Subchondral Bone is the key to develop targeted and effective therapeutic strategies to treat osteochondral defects. The Subchondral Bone consists of the Subchondral Bone plate and the subarticular spongiosa. It is separated by the cement line from the calcified zone of the articular cartilage. A variable anatomy is characteristic for the Subchondral region, reflected in differences in thickness, density, and composition of the Subchondral Bone plate, contour of the tidemark and cement line, and the number and types of channels penetrating into the calcified cartilage. This review aims at providing insights into the anatomy, morphology, and pathology of the Subchondral Bone. Individual diseases affecting the Subchondral Bone, such as traumatic osteochondral defects, osteochondritis dissecans, osteonecrosis, and osteoarthritis are also discussed. A better knowledge of the basic science of the Subchondral region, together with additional investigations in animal models and patients may translate into improved therapies for articular cartilage defects that arise from or extend into the Subchondral Bone.

Joost Geurts - One of the best experts on this subject based on the ideXlab platform.

  • What drives osteoarthritis?—synovial versus Subchondral Bone pathology
    Rheumatology, 2017
    Co-Authors: Thomas Hugle, Joost Geurts
    Abstract:

    Abstract Subchondral Bone and the synovium play an important role in the initiation and progression of OA. MRI often permits an early detection of synovial hypertrophy and Bone marrow lesions, both of which can precede cartilage damage. Newer imaging modalities including CT osteoabsorptiometry and hybrid SPECT-CT have underlined the importance of Bone in OA pathogenesis. The Subchondral Bone in OA undergoes an uncoupled remodelling process, which is notably characterized by macrophage infiltration and osteoclast formation. Concomitant increased osteoblast activity leads to spatial remineralization and osteosclerosis in end-stage disease. A plethora of metabolic and mechanical factors can lead to synovitis in OA. Synovial tissue is highly vascularized and thus exposed to systemic influences such as hypercholesterolaemia or low grade inflammation. This review aims to describe the current understanding of synovitis and Subchondral Bone pathology and their connection in OA.

  • what drives osteoarthritis synovial versus Subchondral Bone pathology
    Rheumatology, 2016
    Co-Authors: Thomas Hugle, Joost Geurts
    Abstract:

    Abstract Subchondral Bone and the synovium play an important role in the initiation and progression of OA. MRI often permits an early detection of synovial hypertrophy and Bone marrow lesions, both of which can precede cartilage damage. Newer imaging modalities including CT osteoabsorptiometry and hybrid SPECT-CT have underlined the importance of Bone in OA pathogenesis. The Subchondral Bone in OA undergoes an uncoupled remodelling process, which is notably characterized by macrophage infiltration and osteoclast formation. Concomitant increased osteoblast activity leads to spatial remineralization and osteosclerosis in end-stage disease. A plethora of metabolic and mechanical factors can lead to synovitis in OA. Synovial tissue is highly vascularized and thus exposed to systemic influences such as hypercholesterolaemia or low grade inflammation. This review aims to describe the current understanding of synovitis and Subchondral Bone pathology and their connection in OA.

Thomas Hugle - One of the best experts on this subject based on the ideXlab platform.

  • What drives osteoarthritis?—synovial versus Subchondral Bone pathology
    Rheumatology, 2017
    Co-Authors: Thomas Hugle, Joost Geurts
    Abstract:

    Abstract Subchondral Bone and the synovium play an important role in the initiation and progression of OA. MRI often permits an early detection of synovial hypertrophy and Bone marrow lesions, both of which can precede cartilage damage. Newer imaging modalities including CT osteoabsorptiometry and hybrid SPECT-CT have underlined the importance of Bone in OA pathogenesis. The Subchondral Bone in OA undergoes an uncoupled remodelling process, which is notably characterized by macrophage infiltration and osteoclast formation. Concomitant increased osteoblast activity leads to spatial remineralization and osteosclerosis in end-stage disease. A plethora of metabolic and mechanical factors can lead to synovitis in OA. Synovial tissue is highly vascularized and thus exposed to systemic influences such as hypercholesterolaemia or low grade inflammation. This review aims to describe the current understanding of synovitis and Subchondral Bone pathology and their connection in OA.

  • what drives osteoarthritis synovial versus Subchondral Bone pathology
    Rheumatology, 2016
    Co-Authors: Thomas Hugle, Joost Geurts
    Abstract:

    Abstract Subchondral Bone and the synovium play an important role in the initiation and progression of OA. MRI often permits an early detection of synovial hypertrophy and Bone marrow lesions, both of which can precede cartilage damage. Newer imaging modalities including CT osteoabsorptiometry and hybrid SPECT-CT have underlined the importance of Bone in OA pathogenesis. The Subchondral Bone in OA undergoes an uncoupled remodelling process, which is notably characterized by macrophage infiltration and osteoclast formation. Concomitant increased osteoblast activity leads to spatial remineralization and osteosclerosis in end-stage disease. A plethora of metabolic and mechanical factors can lead to synovitis in OA. Synovial tissue is highly vascularized and thus exposed to systemic influences such as hypercholesterolaemia or low grade inflammation. This review aims to describe the current understanding of synovitis and Subchondral Bone pathology and their connection in OA.

Daniel Lajeunesse - One of the best experts on this subject based on the ideXlab platform.

  • targeting Subchondral Bone for treating osteoarthritis what is the evidence
    Best Practice & Research: Clinical Rheumatology, 2010
    Co-Authors: Daniel Lajeunesse, Jeanpierre Pelletier, Johanne Martelpelletier
    Abstract:

    Over the past few decades, significant progress has been made with respect to new concepts about the pathogenesis of osteoarthritis (OA). This article summarises some of the knowledge we have today on the involvement of the Subchondral Bone in OA. It provides substantial evidence that changes in the metabolism of the Subchondral Bone are an integral part of the OA disease process and that these alterations are not merely secondary manifestations, but are part of a more active component of the disease. Thus, a strong rationale exists for therapeutic approaches that target Subchondral Bone resorption and/or formation, and data evaluating the drugs targeting Bone remodelling raise the hope that new treatment options for OA may become available.

  • Subchondral Bone in osteoarthritis: a biologic link with articular cartilage leading to abnormal remodeling.
    Current Opinion in Rheumatology, 2003
    Co-Authors: Daniel Lajeunesse, Pascal Reboul
    Abstract:

    This review deals with new findings highlighting the concept of cross-talk between Subchondral Bone tissue and articular cartilage that may be crucial for the initiation and/or progression of osteoarthritis. In this review, new factors either produced by Subchondral Bone tissue or modifying osteoblast metabolism, yet implicated in osteoarthritis, are discussed.

R W Norrdin - One of the best experts on this subject based on the ideXlab platform.

  • the role of Subchondral Bone in joint disease a review
    Equine Veterinary Journal, 2010
    Co-Authors: Christopher E. Kawcak, C W Mcilwraith, R W Norrdin, Richard D Park, Susan P James
    Abstract:

    Summary Subchondral Bone plays a role in the pathogenesis of osteochondral damage and osteoarthritis in horses and humans. Osteochondral fragmentation and fracture, Subchondral Bone necrosis and osteoarthritis are common diseases in athletic horses, and Subchondral Bone is now thought to play an integral role in the pathogenesis of these diseases. There have been numerous research efforts focused on articular cartilage damage and its pathogenesis, yet comparatively little effort focused on Subchondral Bone pathology or the coordinated disease states of the osteochondral tissues. The purpose of this report is to review the current understanding of osteochondral disease in all species and its application to equine research and practice. It can be concluded from this review that our current understanding of osteochondral disease is based on clinical and pathological sources; and that the lack of information about joint tissue adaptation and disease has hampered objective studies of osteochondral tissues.

  • correlation of quantitative computed tomographic Subchondral Bone density and ash density in horses
    Bone, 2009
    Co-Authors: Marti G Drum, C W Mcilwraith, R W Norrdin, Richard D Park, C E Kawcak
    Abstract:

    article The purpose of this study was to compare Subchondral Bone density obtained using quantitative computed tomography with ash density values from intact equine joints, and to determine if there are measurable anatomic variations in mean Subchondral Bone density. Five adult equine metacarpophalangeal joints were scanned with computed tomography (CT), disarticulated, and four 1-cm

  • Subchondral Bone failure in an equine model of overload arthrosis
    Bone, 1998
    Co-Authors: R W Norrdin, Christopher E. Kawcak, B A Capwell, C W Mcilwraith
    Abstract:

    Gross examination of metacarpo-/metatarsophalangeal (fetlock) joints from racehorses revealed defects on the condylar surface that ranged from cartilage fibrillation and erosion to focal cartilage indentations and cavitation in Subchondral Bone characteristic of traumatic osteochondrosis. Because these lesions represented a spectrum of mechanically induced arthrosis in which microdamage is thought to play a role, a histologic study of sagittal sections was made to study the morphogenesis. Subchondral Bone failure developed beneath a flattened section of the condyle where the margin of the sesamoid Bone produces compression as well as shear on impact of the foot with the ground. Milder lesions had thickening of Subchondral Bone and underlying trabeculae. With advancing sclerosis an increased amount of osteocyte necrosis was present. Occasional vascular channels with plugs of matrix debris and cells were present just beneath the cartilage. There was increased prominence of Subchondral vessels, and osteoclastic remodeling was seen in and around the sclerotic zone. Apparent fragmentation lines in the Subchondral Bone suggested increased matrix fragility. Irregular trabecular microfractures developed at a depth of a few millimeters. Increased vascularity with hemorrhage, fibrin, and fibroplasia could be seen in enlarged marrow spaces at this more advanced stage. The overlying articular cartilage was variably indented but remained largely viable with degeneration and erosion limited to the superficial layers. Focally, breaks in the calcified layer appeared to lead to collapse and cartilage infolding. In metacarpal condyles from experimental horses run on a treadmill, there were milder changes at the site. The Subchondral Bone was increased in volume and there was increased diffuse staining with basic fuchsin, but no increase in the number of microcracks was seen. The findings in the racehorses indicate that the equine fetlock condyle is a consistent site of overload arthrosis in which microfracture and failure in Subchondral Bone may occur. Controlled exercise in treadmill horses may provide a model in which to study the pathogenesis.