Changes in articular cartilage and subchondral bone histomorphometry in osteoarthritic knee joints in humans

Bobinac, Dragica; Španjol, Josip; Zoričić, Sanja; Marić, Ivana

doi:10.1016/s8756-3282(02)00982-1

Cited by 257 publications

(228 citation statements)

References 16 publications

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“…These changes are in contrast to those found in human end-stage OA. (4,5,16) However, changes of subchondral bone in experimental guinea pig models at a more advanced stage were found comparable with those in human end-stage OA. (17,18) This suggests that bone remodeling in preclinical animal models of OA is biphasic: an early decrease in trabecular bone volume followed by a phase in which the subchondral bone becomes denser and stiffens.…”

Section: Introductionmentioning

confidence: 75%

Similarities and discrepancies in subchondral bone structure in two differently induced canine models of osteoarthritis

Intema

Sniekers

Weinans

et al. 2010

Journal of Bone and Mineral Research

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In osteoarthritis (OA), cartilage degradation is accompanied by subchondral bone changes. The pathogenesis and physiology of bone changes in OA are still unclear. The changes in subchondral bone architecture and cartilage damage were compared in differently induced experimental models of OA. Experimental OA was induced bilaterally by anterior cruciate ligament transection (ACLT) or by cartilage trauma (Groove model); bilateral sham surgery served as control. Lysylpyridinoline (LP, bone resorption) and C-telopeptide of type II collagen (CTX-II, cartilage breakdown) were measured over time. At 20 weeks after surgery, the subchondral cortical plate and trabecular bone of the tibia were analyzed by micro-computed tomography (mCT) and cartilage degeneration was analyzed histologically and biochemically. In both models, cartilage degeneration and cortical subchondral plate thinning were present. CTX-II levels were elevated over time in both models. Subchondral trabecular bone changes were observed only in the ACLT model, not in the Groove model. Correspondingly, LP levels were elevated over time in the ACLT model and not in the Groove model. Interestingly, the trabecular bone changes in the ACLT model were extended to the metaphyseal area. The early decrease in plate thickness, present in both models, as was cartilage damage, suggests that plate thinning is a phenomenon that is intrinsic to the process of OA independent of the cause/induction of OA. On the other hand, trabecular changes in subchondral and metaphyseal bone are not part of a common pathway of OA development and may be induced biomechanically in the destabilized and less loaded ACLT joint. ß

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Section: Introductionmentioning

confidence: 75%

Similarities and discrepancies in subchondral bone structure in two differently induced canine models of osteoarthritis

Intema

Sniekers

Weinans

et al. 2010

Journal of Bone and Mineral Research

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“…Since this increased density was isolated to 1 region confined to the 2% level, it is possible that some regions of subchondral trabecular bone closer to the cortical plate may experience increased density similar to that of the cortical plate (5,37). Regional variations in the thickness and depth of the cortical plate (46) might have contributed to the finding being limited to this subregion.…”

Section: Discussionmentioning

confidence: 99%

“…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%

“…Regional variations in the thickness and depth of the cortical plate (46) might have contributed to the finding being limited to this subregion. Also, as the disease progresses, changes that may initially occur more proximally, closer to the cortical plate, may extend more distally (37). This may occur at different rates in different regions.…”

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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“…There are no consistently effective methods for preventing OA or slowing its progression, and symptomatic treatments provide limited benefit for many patients. Gross changes in the structure and content of articular cartilage, subchondral bone, synovial membrane, joint ligaments, and tendons have been described for many years in patients with OA (2). However, the molecular changes associated with OA in these tissues have only recently begun to be elucidated (for review, see refs.…”

mentioning

confidence: 99%

Inverse relationship between matrix remodeling and lipid metabolism during osteoarthritis progression in the STR/ORT mouse

Watters¹,

Cheng²,

Pickarski³

et al. 2007

Arthritis & Rheumatism

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Objective. The biologic changes associated with osteoarthritis (OA) are incompletely understood. The aim of this study was to elucidate the molecular mechanisms underlying OA progression in an STR/Ort murine model of spontaneous disease.Methods. Global patterns of gene expression were assessed using microarray analysis of articular cartilage/subchondral bone from the tibial plateaus of STR/Ort mice at 3, 9, and 12 months of age. The age-dependent severity of osteophyte formation and extent of cartilage damage were determined in the corresponding femurs using microfocal computed tomography and the Mankin histologic scoring system. Pathway analysis was used to identify the functions of genes associated with OA progression, and changes in gene expression were confirmed using immunohistochemistry.Results. Six hundred twenty-one genes were associated with both osteophyte formation and cartilage damage in the STR/Ort joints. Genes involved in the development/function of connective tissue and in lipid metabolism were most significantly enriched and regulated during disease progression. Genes directly interacting with peroxisome proliferator-activated receptor ␣ (PPAR␣)/PPAR␥ were down-regulated, whereas those genes involved with connective tissue remodeling were up-regulated during disease progression. Associations of down-regulation of myotubularinrelated phosphatase 1 (a phosphoinositide 3-phosphatase involved in lipid signaling) and up-regulation of biglycan (a member of the small leucine-rich protein family known to modulate osteoblast differentiation and matrix mineralization) with OA progression were confirmed by immunohistochemistry.Conclusion. Since adipogenesis and osteogenesis are inversely related in the developing skeletal tissue, these results suggest that a shift in the differentiation of mesenchymal cells from adipogenesis toward osteogenesis is a component of the OA pathophysiologic processes occurring in the tibial plateau joints of STR/Ort mice.

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Changes in articular cartilage and subchondral bone histomorphometry in osteoarthritic knee joints in humans

Cited by 257 publications

References 16 publications

Similarities and discrepancies in subchondral bone structure in two differently induced canine models of osteoarthritis

Similarities and discrepancies in subchondral bone structure in two differently induced canine models of osteoarthritis

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

Inverse relationship between matrix remodeling and lipid metabolism during osteoarthritis progression in the STR/ORT mouse

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