Estrogen Receptor-β Is the Predominant Estrogen Receptor Subtype in Normal Human Synovia

Dietrich, Wulf; Haitel, Andrea; Holzer, Gerold; Huber, Johannes; Kolbus, Andrea; Tschugguel, Walter

doi:10.1016/j.jsgi.2006.07.002

Cited by 45 publications

(36 citation statements)

References 34 publications

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“…Previous studies have identified estrogen receptors on most joint components, including cartilage, bone, ligaments, and synovium 18–22 , indicating a regulatory role for estrogen in these tissues. Because cartilage damage is the major radiological and pathological manifestation observed in joint degeneration, several studies have explored the influence of estrogen on cartilage metabolism.…”

Section: Discussionmentioning

confidence: 99%

Estrogen deficiency accelerates lumbar facet joints arthritis

Chen

Zhu

Zhang

et al. 2017

Sci Rep

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Dramatic increase in the prevalence of lumbar facet joint (LFJ) arthritis in women around the age of menopause indicates a protective role for estrogen in LFJ arthritis. To date, there is no evidence for this indication and the mechanism of such an effect remains poorly understood. In this study, ovariectomized (OVX) mice were used to mimic the estrogen-deficient status of post-menopausal women. Micro-CT and immunohistochemistry was employed to assess the morphological and molecular changes in ovariectomy-induced LFJ arthritis. The results show that the LFJ subchondral bone mass was significantly decreased in OVX mice, with increased cavities on the interface of the subchondral bone. Severe cartilage degradation was observed in ovariectomy-induced LFJ arthritis. Increased blood vessels and innervations were also found in degenerated LFJ, particularly in the subchondral bone area. 17β-Estradiol treatment efficiently suppressed LFJ subchondral bone turnover, markedly inhibited cartilage degradation, and increased blood vessel and nerve ending growth in degenerated LFJ in OVX mice. Our study reveals that estrogen is a key factor in regulating LFJ metabolism. Severe LFJ degeneration occurs when estrogen is absent in vivo. Collapsed subchondral bone may be the initiation of this process, and estrogen replacement therapy can effectively prevent degeneration of LFJ under estrogen-deficient conditions.

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Section: Discussionmentioning

confidence: 99%

Estrogen deficiency accelerates lumbar facet joints arthritis

Chen

Zhu

Zhang

et al. 2017

Sci Rep

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“…In articular tissues, both ER types are expressed by the chondrocytes [10], subchondral bone cells [11], synoviocytes [12], ligament fibroblasts [13] and myoblasts [14] in humans and other species. However, ERα is predominant in cortical bone and ERβ predominates in cartilage, cancellous bone and synovium [10,12,68].…”

Section: Mechanisms Underlying the Effects Of Estrogen On Joint Tissuesmentioning

confidence: 99%

Osteoarthritis associated with estrogen deficiency

et al. 2009

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Osteoarthritis (OA) affects all articular tissues and finally leads to joint failure. Although articular tissues have long been considered unresponsive to estrogens or their deficiency, there is now increasing evidence that estrogens influence the activity of joint tissues through complex molecular pathways that act at multiple levels. Indeed, we are only just beginning to understand the effects of estrogen deficiency on articular tissues during OA development and progression, as well as on the association between OA and osteoporosis. Estrogen replacement therapy and current selective estrogen receptor modulators have mixed effectiveness in preserving and/or restoring joint tissue in OA. Thus, a better understanding of how estrogen acts on joints and other tissues in OA will aid the development of specific and safe estrogen ligands as novel therapeutic agents targeting the OA joint as a whole organ.

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“…Abundant expression of ERβ compared with ERα has been reported in synovial membrane. 31 The existence of two subtypes of ER expression provides one line of evidence that cartilage and synovium are indeed sensitive to estrogens. Chondrocytes are known to endogenously produce estradiol (E2) and it is also known that locally produced E2 stimulates chondrocyte proliferation and confers protection against spontaneous apoptosis.…”

Section: Osteoporosis and Fracturesmentioning

confidence: 99%

Safety profiles of aromatase inhibitors and selective estrogen-receptor modulators in the treatment of early breast cancer

Yamamoto

Iwase

2008

Int J Clin Oncol

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For the medical treatment of early breast cancer, aromatase inhibitors (AIs) such as anastrozole, letrozole, and exemestane are more effective than selective estrogen-receptor modulators (SERMs) such as tamoxifen (TAM). However, the adverse events associated with AIs are different from those associated with SERMs. Hot flushes, gynecological disorders, and thrombosis are more frequent in patients treated with TAM than in those treated with AIs. Conversely, osteoporosis, fractures, joint symptoms, and myalgia are more common in patients receiving AIs. Osteoporosis and bone fractures resulting from osteoporosis are important issues for patients treated with AIs. The precise management of bone health, in strict accordance with clinical guidelines, is vital in patients receiving AIs. AI-related joint symptoms are also one of the most important considerations for patients taking AIs. AI-related joint symptoms are the most common reason for the discontinuation of AIs. Confirmed management strategies for AI-related joint symptoms are unavailable at present. In patients receiving AIs, long-term adverse events (for example, those occurring as a result of changing lipid metabolism) remain unclear. There is a clear need to elucidate AI-related adverse events over the long term and to establish management strategies for AI-related adverse events, such that AIs can be used safely in patients with breast cancer over long periods of time.

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Estrogen Receptor-β Is the Predominant Estrogen Receptor Subtype in Normal Human Synovia

Abstract: In view of our observation that ER beta but not ER alpha is expressed regularly in normal human synovia in high amounts, we propose that estrogen could play a significant role in synovial membrane function in women and men, operating preferably via the ER beta isoform.

Cited by 45 publications

References 34 publications

Estrogen deficiency accelerates lumbar facet joints arthritis

Estrogen deficiency accelerates lumbar facet joints arthritis

Osteoarthritis associated with estrogen deficiency

Safety profiles of aromatase inhibitors and selective estrogen-receptor modulators in the treatment of early breast cancer

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