The effect on cartilage of different forms of application of postmenopausal estrogen therapy: comparison of oral and transdermal therapy

Ravn, Pernille; Warming, Lise; Stephan, Carsten; Christiansen, Claus

doi:10.1016/j.bone.2004.07.017

Cited by 36 publications

(26 citation statements)

References 19 publications

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“…No previous studies have examined the effects of antiresorptive drug use on COMP level in postmenopausal women with osteopenia or osteoporosis. In the present study, estrogen significantly reduced the serum levels of COMP in postmenopausal women, supporting the notion that estrogen therapy might have a chondroprotective effect on OA progression [16,23]. Our data were in line with a previous study indicating that oral and transdermal estradiol had an effect on cartilage turnover reflected in a decrease of about 25% in urinary concentration of collagen type II C-telopeptide degradation products (CTX-II) in healthy postmenopausal women [23].…”

Section: Discussionsupporting

confidence: 67%

“…In the present study, estrogen significantly reduced the serum levels of COMP in postmenopausal women, supporting the notion that estrogen therapy might have a chondroprotective effect on OA progression [16,23]. Our data were in line with a previous study indicating that oral and transdermal estradiol had an effect on cartilage turnover reflected in a decrease of about 25% in urinary concentration of collagen type II C-telopeptide degradation products (CTX-II) in healthy postmenopausal women [23]. Treatment of postmenopausal women with a selective-estrogen receptor modulator (SERM) also caused a decrease in CTX-II, suggesting potential therapeutic benefits of SERM in the prevention of destructive joint diseases [24].…”

Section: Discussionsupporting

confidence: 67%

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Changes in Serum Levels of Cartilage Oligomeric Matrix Protein after Estrogen and Alendronate Therapy in Postmenopausal Women

Seo

Yang²,

Lim³

et al. 2012

Gynecol Obstet Invest

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Background: Cartilage oligomeric matrix protein (COMP) is a biomarker for joint destruction and its serum levels are used for assessing therapeutic efficacy. This study aims to compare changes in serum COMP levels in postmenopausal women with osteopenia/osteoporosis receiving estrogen and alendronate. Methods: A total of 62 postmenopausal women diagnosed with osteopenia or osteoporosis were treated with either estrogen (17β-estradiol 1 mg, n = 30) or bisphosphonate (alendronate 5 mg, n = 32) for 6 months. The controls were healthy postmenopausal women (n = 30). Serum COMP and osteocalcin levels were measured at baseline and after 6 months of treatment. Results: Estrogen decreased levels of COMP at 6 months compared to baseline levels (–8.35 ± 19.38%), whereas the bisphosphonate and control groups resulted in no significant changes (–5.50 ± 18.69 and –1.49 ± 25.34%, respectively). Concentrations of osteocalcin decreased significantly in both treatment groups (estrogen –25.60 ± 24.42% and alendronate –13.76 ± 23.89%, respectively). There was a significant positive correlation between changes after 6 months in COMP and osteocalcin (R = 0.48, p = 0.002). Conclusions: Postmenopausal women treated with estrogen showed significantly decreased levels of COMP after 6 months. Estrogen might provide a further treatment modality in the prevention of joint destruction.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionsupporting

confidence: 67%

Changes in Serum Levels of Cartilage Oligomeric Matrix Protein after Estrogen and Alendronate Therapy in Postmenopausal Women

Seo

Yang²,

Lim³

et al. 2012

Gynecol Obstet Invest

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“…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). These data collectively suggest that collagen degradation, synthesis, deposition and processing are important in integrative cartilage repair.…”

supporting

confidence: 63%

“…Furthermore, integration between cell-seeded matrices and articular cartilage is inhibited relative to unseeded matrices or devitalized articular cartilage (Giurea et al, 2002;Peretti et al, 2006). We have noted similar occurrences with combinations of live and dead neocartilages grown in opposition, arguing that this inhibitory phenomenon is not limited to native cartilages (Redman et al, 2005 Cartilage integration precultured devitalized ovine cartilage slices with isolated chondrocytes then recombined slices with fibrin glue and implanted them into nude mice for up to 42 days (Peretti et al, 1998). Bonding of cartilage slices occurred in all samples that were precultured with chondrocytes prior to implantation but never in the absence of cells.…”

mentioning

confidence: 53%

“…In the ideal scenario the repair process and restored tissue are biological in origin, but complete cartilage degeneration necessitates total joint replacement through artificial implants. In most cases clinical intervention has the greatest benefit for symptomatic lesions which are small enough to be filled with cells and repair tissue from various sources (Redman et al, 2005). At the very least the repair tissue should replicate the biomechanical function of the surrounding normal cartilage, allow pain-free articulation, integrate with surrounding host tissue, and prevent further cartilage degeneration.…”

Section: Methods Of Cartilage Repairmentioning

confidence: 99%

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

Englert

Blunk

Fierlbeck

et al. 2006

Arthritis & Rheumatism

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Objective. Posttraumatic integration of articular cartilage at fracture sites is essential for mechanical stability of cartilage, and ruptured cartilage is a prerequisite for early osteoarthritis. This study was undertaken to investigate effects on articular cartilage integration mediated by steroid hormones, interleukin-1␤ (IL-1␤), and combinations thereof.Methods. Articular cartilage blocks were cultured in partial apposition for 2 weeks with ascorbic acid, testosterone, 17␤-estradiol, and dehydroepiandrosterone (DHEA), with or without IL-1␤. Mechanical integration was measured as adhesive strength, i.e., the maximum force at rupture of integrated cartilage blocks divided by the overlap area. Glycosaminoglycan content was used to study synthesized extracellular matrix.Results. Culture in medium without supplements did not lead to integration (adhesive strength 0 kPa). With administration of ascorbic acid (100 g/ml), the median adhesive strength was 49 kPa. In comparison with ascorbic acid alone, all steroid hormones induced a strong, concentration-dependent stimulation of integration (with maximum values observed with DHEA at 3 ؋ 10 ؊5 M, testosterone at 10 ؊8 M, and 17␤-estradiol at 10 ؊11 M). For testosterone and 17␤-estradiol, this was also reflected by an increase of glycosaminoglycan content. Adhesive strength was increased with IL-1␤ at 10 pg/ml, but not at 1 pg/ml or 100 pg/ml. In the presence of both IL-1␤ and sex hormones, integration of articular cartilage was reduced.Conclusion. This is the first study to demonstrate that steroid hormones such as 17␤-estradiol, DHEA, and testosterone stimulate articular cartilage integration. This effect is abrogated by low concentrations of IL-1␤. In the absence of IL-1␤ or after neutralization of IL-1␤, steroid hormones might be favorable adjuvant compounds to optimize cartilage integration.

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The effect on cartilage of different forms of application of postmenopausal estrogen therapy: comparison of oral and transdermal therapy

Cited by 36 publications

References 19 publications

Changes in Serum Levels of Cartilage Oligomeric Matrix Protein after Estrogen and Alendronate Therapy in Postmenopausal Women

Changes in Serum Levels of Cartilage Oligomeric Matrix Protein after Estrogen and Alendronate Therapy in Postmenopausal Women

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

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

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