The involvement of subchondral mineralized tissues in osteoarthrosis: Quantitative microscopic evidence

Burr, David B.; Schaffler, Mitchell B.

doi:10.1002/(sici)1097-0029(19970515)37:4<343::aid-jemt9>3.0.co;2-l

Cited by 210 publications

(127 citation statements)

References 76 publications

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“…The exact effect depends on the relative magnitude and direction of the changes in bone volume and material density, although only to the extent that these change bone mass (given that total volume is fixed in vBMD). Studies that have shown an increase in subchondral trabecular bone (e.g., BV/TV) have also generally investigated the region very close to the subchondral cortical plate (36)(37)(38). A reduction in bone may be more characteristic of trabecular bone at a greater distance from the cortical plate (5,38).…”

Section: Discussionmentioning

confidence: 99%

“…This may, in turn, reduce the stiffness of the cortical plate (42)(43)(44). However, the timing of these cortical plate changes is complex and not particularly well understood (3,38). However, it has been suggested that the thickened but less stiff cortical bone would absorb more of the load through the knee joint, thus potentially shielding the underlying subchondral trabecular bone (2,3,5,13).…”

Section: Discussionmentioning

confidence: 99%

“…However, given that our results were seen in those with more advanced disease, this is a less likely explanation. Regardless of the mechanism, the timing of these reductions in bone density is also not well understood (3,6,13,38).…”

Section: Discussionmentioning

confidence: 99%

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Tibial subchondral trabecular volumetric bone density in medial knee joint osteoarthritis using peripheral quantitative computed tomography technology

Bennell¹,

Creaby²,

Wrigley³

et al. 2008

Arthritis & Rheumatism

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Objective. Knee osteoarthritis (OA) is an organlevel failure of the joint involving pathologic changes in articular cartilage and bone. This cross-sectional study compared apparent volumetric bone mineral density (vBMD) of proximal tibial subchondral trabecular bone in people with and without knee OA, using peripheral quantitative computed tomography (pQCT).Methods. Seventy-five individuals with mild or moderate medial compartment knee OA and 41 asymptomatic controls were recruited. Peripheral QCT was used to measure vBMD of trabecular bone beneath medial and lateral tibiofemoral compartments at levels of 2% and 4% of tibial length, distal to the tibial plateau.Results. There was no significant difference in vBMD beneath the overall medial and lateral compartments between the 3 groups. However, in the affected medial compartment of those with moderate OA, lower vBMD was seen in the 2 posterior subregions compared with controls and those with mild knee OA, while higher vBMD was seen in the anteromedial subregion. Beneath the unaffected or lesser affected lateral compartment, significantly lower vBMD was seen at the 2% level in the anterior and lateral subregions of those with moderate disease. Volumetric BMD ratios showed relatively higher vBMD in the medial compartment compared with the lateral compartment, but these ratios were not influenced by disease status.Conclusion. Subregional vBMD changes were evident beneath the medial and lateral compartments of those with moderate medial knee OA. Of import, the posterior subchondral trabecular regions of the medial tibial plateau have markedly lower vBMD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Tibial subchondral trabecular volumetric bone density in medial knee joint osteoarthritis using peripheral quantitative computed tomography technology

Bennell¹,

Creaby²,

Wrigley³

et al. 2008

Arthritis & Rheumatism

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“…Hence, subchondral bone tissue may, through the production of cytokines, growth factors and eicosanoids, induce OA cartilage degradation [98][99][100]. Interestingly, in addition to the subchondral bone cells, the OPG/RANK/RANKL molecular triad has also been observed to be expressed and produced by another articular cell, the chondrocyte.…”

Section: Potential Factors In Subchondral Bone/cartilage Cross-talkmentioning

confidence: 99%

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

Tat

Lajeunesse

Pelletier

et al. 2010

Best Practice & Research Clinical Rheumatology

157

121

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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.

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“…The functional integrity of the articular cartilage can therefore depend on the mechanical properties of the underlying bone. Accordingly, cartilage damage leads to full-thickness cartilage loss only upon repetitive loading over an already stiffened subchondral bone plate (3).…”

mentioning

confidence: 99%

The role of subchondral bone remodeling in osteoarthritis: Reduction of cartilage degeneration and prevention of osteophyte formation by alendronate in the rat anterior cruciate ligament transection model

Hayami

Pickarski

Wesolowski

et al. 2004

Arthritis & Rheumatism

514

466

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Objective. It has been suggested that subchondral bone remodeling plays a role in the progression of osteoarthritis (OA). To test this hypothesis, we characterized the changes in the rat anterior cruciate ligament transection (ACLT) model of OA and evaluated the effects of alendronate (ALN), a potent inhibitor of bone resorption, on cartilage degradation and on osteophyte formation.Methods. Male Sprague-Dawley rats underwent ACLT or sham operation of the right knee. Animals were then treated with ALN (0.03 and 0.24 g/kg/week subcutaneously) and necropsied at 2 or 10 weeks postsurgery. OA changes were evaluated. Subchondral bone volume and osteophyte area were measured by histomorphometric analysis. Coimmunostaining for transforming growth factor ␤ (TGF␤), matrix metalloproteinase 9 (MMP-9), and MMP-13 was performed to investigate the effect of ALN on local activation of TGF␤.Results. ALN was chondroprotective at both dosages, as determined by histologic criteria and collagen degradation markers. ALN suppressed subchondral bone resorption, which was markedly increased 2 weeks postsurgery, and prevented the subsequent increase in bone formation 10 weeks postsurgery, in the untreated tibial plateau of ACLT joints. Furthermore, ALN reduced the incidence and area of osteophytes in a dosedependent manner. ALN also inhibited vascular invasion into the calcified cartilage in rats with OA and blocked osteoclast recruitment to subchondral bone and osteophytes. ALN treatment reduced the local release of active TGF␤, possibly via inhibition of MMP-13 expression in articular cartilage and MMP-9 expression in subchondral bone. Conclusion. Subchondral bone remodeling plays an important role in the pathogenesis of OA. ALN or other inhibitors of bone resorption could potentially be used as disease-modifying agents in the treatment of OA.Osteoarthritis (OA) is a degenerative joint disease characterized by pain, cartilage loss, and joint stiffness. Although OA has long been considered to be primarily a cartilage disorder associated with focal articular cartilage degradation, this disease is accompanied by well-defined changes in the subchondral and periarticular bone, including sclerosis and cyst and osteophyte formation (1). The importance of the bone changes in the initiation and progression of OA is still being debated. It has been suggested that increased subchondral bone stiffness reduces the ability to dissipate the load and distribute the strain generated within the joint. This increases peak dynamic forces in the overlying articular cartilage and can accelerate its damage over time (2). The functional integrity of the articular cartilage can therefore depend on the mechanical properties of the underlying bone. Accordingly, cartilage damage leads to full-thickness cartilage loss only upon repetitive loading over an already stiffened subchondral bone plate (3).Recent studies have demonstrated increased subchondral bone turnover accompanied by specific architectural changes in the subchondral trabecular bone in OA joints (4,5...

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The involvement of subchondral mineralized tissues in osteoarthrosis: Quantitative microscopic evidence

Cited by 210 publications

References 76 publications

Tibial subchondral trabecular volumetric bone density in medial knee joint osteoarthritis using peripheral quantitative computed tomography technology

Tibial subchondral trabecular volumetric bone density in medial knee joint osteoarthritis using peripheral quantitative computed tomography technology

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

The role of subchondral bone remodeling in osteoarthritis: Reduction of cartilage degeneration and prevention of osteophyte formation by alendronate in the rat anterior cruciate ligament transection model

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