Steroid hormones strongly support bovine articular cartilage integration in the absence of interleukin‐1β

Englert, Carsten; Blunk, Torsten; Fierlbeck, J.; Kaiser, Julia; Stosiek, Wolfgang; Angele, Peter; Hammer, J.; Straub, Rainer H.

doi:10.1002/art.22250

Cited by 23 publications

(20 citation statements)

References 35 publications

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“…A study examined the effects of steroid hormones in bovine cartilage that is lacking a known inhibitor to integration, interleukin-1β. An increase of ∼50 kPa in mechanical integration was seen [31], as compared to the 700 kPa obtained in this study for the native-to-native controls. Also, it has also been shown that, without the assistance of exogenous agents, strength of half that which is seen in intact cartilage can be achieved in an equine model for chondrocyte transplantation [32].…”

Section: Discussionsupporting

confidence: 44%

Induced Collagen Cross-Links Enhance Cartilage Integration

Athens

Makris

2013

PLoS ONE

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Articular cartilage does not integrate due primarily to a scarcity of cross-links and viable cells at the interface. The objective of this study was to test the hypothesis that lysyl-oxidase, a metalloenzyme that forms collagen cross-links, would be effective in improving integration between native-to-native, as well as tissue engineered-to-native cartilage surfaces. To examine these hypotheses, engineered cartilage constructs, synthesized via the self-assembling process, as well as native cartilage, were implanted into native cartilage rings and treated with lysyl-oxidase for varying amounts of time. For both groups, lysyl-oxidase application resulted in greater apparent stiffness across the cartilage interface 2–2.2 times greater than control. The construct-to-native lysyl-oxidase group also exhibited a statistically significant increase in the apparent strength, here defined as the highest observed peak stress during tensile testing. Histology indicated a narrowing gap at the cartilage interface in lysyl-oxidase treated groups, though this alone is not sufficient to indicate annealing. However, when the morphological and mechanical data are taken together, the longer the duration of lysyl-oxidase treatment, the more integrated the interface appeared. Though further data are needed to confirm the mechanism of action, the enhancement of integration may be due to lysyl-oxidase-induced pyridinoline cross-links. This study demonstrates that lysyl-oxidase is a potent agent for enhancing integration between both native-to-native and native-to-engineered cartilages. The fact that interfacial strength increased manifold suggests that cross-linking agents should play a significant role in solving the difficult problem of cartilage integration. Future studies must examine dose, dosing regimen, and cellular responses to lysyl-oxidase to optimize its application.

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Section: Discussionsupporting

confidence: 44%

Induced Collagen Cross-Links Enhance Cartilage Integration

Athens

Makris

2013

PLoS ONE

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“…Collagenase digest accelerates implanted cartilage slice integration, accelerating the formation of a biomechanically stable tissue, but also facilitating chondrocyte outgrowth causing chondrocytes to migrate and colonise the remaining scaffold, enhancing both vertical and lateral integration. Steroid hormones such as dihydroepiandrosterone and 17β-estradiol have also been shown to strongly support in vitro cartilage:cartilage integration in a dose-dependent manner, that is thought to be related to an anabolic response related to collagen turnover (Englert et al, 2006). In support of the latter finding, the fact that in post-menopausal women replacement hormone therapy causes a significant decrease in urine C-telopeptides of type II collagen is thought to be relevant (Ravn et al, 2004).…”

mentioning

confidence: 91%

Evaluation of the reasons for failure of integration during cartilage repair. A review

Khan¹,

Gilbert²,

Singhrao³

et al. 2008

eCM

245

221

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Articular cartilage is a challenging tissue to reconstruct or replace principally because of its avascular nature; large chondral lesions in the tissue do not spontaneously heal. Where lesions do penetrate the bony subchondral plate, formation of hematomas and the migration of mesenchymal stem cells provide an inferior and transient fibrocartilagenous replacement for hyaline cartilage. To circumvent the poor intrinsic reparative response of articular cartilage several surgical techniques based on tissue transplantation have emerged. One characteristic shared by intrinsic reparative processes and the new surgical therapies is an apparent lack of lateral integration of repair or graft tissue with the host cartilage that can lead to poor prognosis. Many factors have been cited as impeding cartilage:cartilage integration including; chondrocyte cell death, chondrocyte dedifferentiation, the nature of the collagenous and proteoglycan networks that constitute the extracellular matrix, the type of biomaterial scaffold employed in repair and the origin of the cells used to repopulate the defect or lesion. This review addresses the principal intrinsic and extrinsic factors that impede integration and describe how manipulation of these factors using a host of strategies can positively influence cartilage integration. Keywords IntroductionArticular cartilage is a highly organised avascular and aneural tissue that provides a smooth surface for the movement of articulating bones and transmission of loads (Muir, 1995). Cartilage carries out the latter function by transferring the forces generated by locomotion to the underlying bone. The resident cells of articular cartilage are chondrocytes that are surrounded by an extensive extracellular matrix whose primary constituents are water, aggrecans and type II collagen. Aggrecans are rich in covalently bonded glycosaminoglycans that are hydrophilic and whose electronegative properties resist applied compressive forces. The tensile strength required to constrain the electronegative force generated by the aggrecans is provided by an organised network of crosslinked fibrils principally containing type II collagen. In cross-section articular cartilage displays a pseudostratified appearance composed of three unmineralised layers; the superficial zone with small, dicoidal chondrocytes aligned parallel to the surface, a transitional zone where chondrocytes are rounded with no apparent organisation and the radial/deep zone where large chondrocytes are aligned in columns of 4-6 cells at right-angles to the surface, Figure 1. The fourth layer is the calcified zone where mineralisation is restricted to the interterritorial matrix of chondrocytes. The calcified zone borders and interdigitates with the subchondral bone. Cartilage defects TraumaIn younger patients who have generally suffered trauma to a joint, focal lesions may appear that if untreated may lead to further progressive degeneration over time. Clinically, focal lesions are graded from the appearance of superficial fissure...

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“…S. Hanna et al, 2007). Steroid hormones have been found to counterbalance catabolic chondrocyte metabolism and counteract proinflammatory effects of catabolic cytokines such as interleukin-1β, interleukin-6, and tumor necrosis factor (Englert et al, 2006). In male rabbits, castration results in an increase in apoptosis and a decrease in the proliferation of the chondrocytes in the growth plate (Irie, Aizawa, & Kokubun, 2005).…”

Section: Commentsmentioning

confidence: 99%

Increased Femoral Cartilage Thickness in Patients With Klinefelter Syndrome

et al. 2012

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The objective of this study was to determine femoral cartilage thickness (FCT) in patients with Klinefelter syndrome (KS), which is the most common sex chromosome disorder in men with varying degrees of androgen deficiency. This cross-sectional controlled study was conducted in a tertiary care center. Participants were 33 male patients (mean age = 36.2 years) with KS and 35 aged-matched healthy male controls (mean age = 32.9 years). Femoral condyle cartilage was measured by ultrasonography at three locations in each knee. Total testosterone, estradiol, sex hormone binding globulin, free androgen index, bioavailable testosterone, and albumin levels were measured. Femoral cartilage of patients at right and left knee lateral (3.03 and 2.99 mm), mid (3.81 and 3.74 mm), and medial (3.01 and 3.20 mm) were statistically thicker than in controls (right and left knee lateral 2.29 and 2.36 mm, mid 2.64 and 2.53 mm, medial 2.39 and 2.32 mm, respectively, p < .001). There was no significant correlation between FCT and sex hormones. In conclusion, patients with KS had thicker femoral cartilage. Relatively low testosterone levels in these patients and altered estrogen metabolism may hypothetically explain increased cartilage thickness in these patients.

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Steroid hormones strongly support bovine articular cartilage integration in the absence of interleukin‐1β

Cited by 23 publications

References 35 publications

Induced Collagen Cross-Links Enhance Cartilage Integration

Induced Collagen Cross-Links Enhance Cartilage Integration

Evaluation of the reasons for failure of integration during cartilage repair. A review

Increased Femoral Cartilage Thickness in Patients With Klinefelter Syndrome

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