Expression of genes for estrogen receptors α and β in human articular chondrocytes

Ushiyama, Toshio; Ueyama, Hisao; Inoue, Koji; Ohkubo, Iwao; Hukuda, Sinsuke

doi:10.1053/joca.1999.0260

Cited by 172 publications

(105 citation statements)

References 36 publications

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“…Recent animal studies have implicated estrogen as a potential mediator of degradative TMJ remodeling, such as decreased bone volume and osteophyte formation 17,25 . Estrogen receptors (ER), through which estrogen performs its biologic function, have been identified in the articular cartilage and growth plate 7,21 . This has directed research on the ability of cartilage to respond to estrogen in terms of cartilage homeostasis and linear bone growth 14,19 .…”

mentioning

confidence: 99%

Estrogen receptor gene polymorphism and craniofacial morphology in female TMJ osteoarthritis patients

Lee

Kim

Kang

et al. 2006

International Journal of Oral and Maxillofacial Surgery

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mentioning

confidence: 99%

Estrogen receptor gene polymorphism and craniofacial morphology in female TMJ osteoarthritis patients

Lee

Kim

Kang

et al. 2006

International Journal of Oral and Maxillofacial Surgery

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“…Several in vivo [25] and in vitro [26] studies have demonstrated that cartilage is an estrogen-sensitive tissue. Both isoforms of estrogen receptors (ERs), ERa and ERh, are present in chondrocytes from humans [27] and animals [28]. In vitro studies showed that soy protein, regardless of isoflavone content, because of the other components (e.g., soybean unsaponifiables) inhibits pro-inflammatory cytokines in chondrocytes [29].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of soy protein on collagen-induced arthritis in rat

et al. 2011

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To evaluate preventive and therapeutic effects of soy protein on collagen-induced arthritis rats. Sprague-Dawley rats immunized with bovine type II collagen emulsified in adjuvant and treated with soy protein (7 g/kg), dexamethasone (1 mg/kg), and casein (in control groups) by daily gavages feedings for 30 days. Score of arthritis recorded every day for each paws of animal. Tumor necrosis factor-alpha, interleukin6, leptin, and adiponectin were measured in serums. Treatment with soy protein resulted in significant delay in time to onset of arthritis as well as significantly decreased arthritis incidence, clinical arthritis severity score, histopathological arthritis severity score, and in vivo cell-mediated immunity to collagen (P < 0.05). Administration of soy protein significantly suppressed the progression of collagen II-induced arthritis and inhibited the production of tumor necrosis factor-alpha, interleukin6, leptin, and adiponectin. Soy protein appeared to be a potent immunomodulatory inhibitor of collagen II-induced arthritis in rats. It could delay onset of RA and reduced cartilage erosion and synovitis inflammation. Therefore, it may be a useful protein in the prevention and treatment of rheumatoid arthritis patient.

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“…Estrogens modulate local inflammation in various disorders of the joint via synoviocytes and chondrocytes [17]. Synovial fibroblasts are responsible for matrix protein production.…”

Section: Pathophysiological Considerationsmentioning

confidence: 99%

“…Furthermore, androstenedione is converted to estrone and estradiol in synoviocytes. The identification of estrogen receptors a and b in chondrocytes implies a possible biological link between joint cartilage effects and estrogen deprivation [17,18]. It has been shown that estrogen-associated variations in the activity of l-opioid neurotransmission correlated with individual ratings of both the sensory and affective perceptions of pain [16].…”

Section: Pathophysiological Considerationsmentioning

confidence: 99%

Musculoskeletal events associated with the management of endocrine-responsive breast cancer

et al. 2010

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Musculoskeletal symptoms have been reported in patients treated with third generation aromatase inhibitors (AIs) and with blockers of hypothalamic-pituitary gonadal axis. AIs act by suppressing postmenopausal estrogen biosynthesis through inhibition of the enzyme aromatase, which is responsible for the conversion of androgens to estrogens in many tissues. Maximal estrogen and/or androgen deprivation is beneficial for cancer growth suppression but could be associated with side effects such as accelerated bone loss and osteoporotic fractures which are extensively reported. Musculoskeletal events, another group of adverse events, have been studied to a lesser extent and are usually commonly reported as arthralgia and myalgia. Furthermore, the pathogenesis and anatomical findings of musculoskeletal symptoms have not been adequately elucidated. In this communication, we review recent information related to musculoskeletal symptoms in breast cancer and speculate on possible explanations for musculoskeletal pain related to hormone deprivation. We outline treatment options for control of arthralgia and myalgia due to hormonal therapy. More knowledge about the etiology and management of musculoskeletal adverse effects breast cancer during endocrine therapy is needed because discontinuation of the treatment due to intolerant symptomatology may result in disruption of the treatment schedule.

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Expression of genes for estrogen receptors α and β in human articular chondrocytes

Cited by 172 publications

References 36 publications

Estrogen receptor gene polymorphism and craniofacial morphology in female TMJ osteoarthritis patients

Estrogen receptor gene polymorphism and craniofacial morphology in female TMJ osteoarthritis patients

Protective effect of soy protein on collagen-induced arthritis in rat

Musculoskeletal events associated with the management of endocrine-responsive breast cancer

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