Oestrogen exhibits type II collagen protective effects and attenuates collagen-induced arthritis in rats

Nielsen, Rasmus Hjorth; Christiansen, Claus; Stolina, Marina; Karsdal, Morten A.

doi:10.1111/j.1365-2249.2008.03594.x

Cited by 37 publications

(46 citation statements)

References 36 publications

(45 reference statements)

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“…10,49 However, estrogen has been shown to protect against CIA in DBA/ 1LacJ mice and Lewis rats. 94,95 What could account for this discrepancy? One possibility is that the acute inflammation including macrophages and neutrophils that is induced by CFA/collagen in the CIA model is inhibited by estrogen, as discussed in the previous section.…”

Section: Rheumatoid Arthritis: Acute Mixed Cell and Antibody-mediatedmentioning

confidence: 99%

Sex Differences in Autoimmune Disease from a Pathological Perspective

Fairweather

Frisancho-Kiss

Rose

2008

The American Journal of Pathology

513

418

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Autoimmune diseases affect ϳ8% of the population, 78% of whom are women. The reason for the high prevalence in women is unclear. Women are known to respond to infection, vaccination, and trauma with increased antibody production and a more T helper (Th)2-predominant immune response, whereas a Th1 response and inflammation are usually more severe in men. This review discusses the distribution of autoimmune diseases based on sex and age, showing that autoimmune diseases progress from an acute pathology associated with an inflammatory immune response to a chronic pathology associated with fibrosis in both sexes. Autoimmune diseases that are more prevalent in males usually manifest clinically before age 50 and are characterized by acute inflammation, the appearance of autoantibodies, and a proinflammatory Th1 immune response. In contrast, femalepredominant autoimmune diseases that manifest during the acute phase, such as Graves' disease and systemic lupus erythematosus, are diseases with a known antibody-mediated pathology. Autoimmune diseases with an increased incidence in females that appear clinically past age 50 are associated with a chronic, fibrotic Th2-mediated pathology. Th17 responses increase neutrophil inflammation and chronic fibrosis. This distinction between acute and chronic pathology has primarily been overlooked, but greatly impacts our understanding of sex differences in autoimmune disease. Autoimmune diseases are the third most common category of disease in the United States after cancer and cardiovascular disease, affecting ϳ5 to 8% of the population or 14.7 to 23.5 million people.1 Conservative estimates indicate that ϳ78% of the people affected with autoimmune diseases are women.2-4 For some time it has been known that the basic immune response differs between men and women. Women respond to infection, vaccination, and trauma with increased antibody production, whereas inflammation is usually more severe in men resulting in an increased mortality in men and protection against infection in women. [5][6][7][8][9][10]

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Section: Rheumatoid Arthritis: Acute Mixed Cell and Antibody-mediatedmentioning

confidence: 99%

Sex Differences in Autoimmune Disease from a Pathological Perspective

Fairweather

Frisancho-Kiss

Rose

2008

The American Journal of Pathology

513

418

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“…There is also some evidence that oral contraceptives have a protective role in RA 33 . In animal models, estrogen treatment delayed disease onset and reduced the degree of cartilage degradation in rats with collagen-induced arthritis 34 .…”

Section: Estrogens and Rheumatoid Arthritismentioning

confidence: 99%

The effects of hormone replacement therapy on autoimmune disease: rheumatoid arthritis and systemic lupus erythematosus

Holroyd

Edwards

2009

Climacteric

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Autoimmune diseases are generally more common in women than men; however, there is no simple explanation for this. Sex hormones, especially estrogen (but also prolactin and testosterone), play important roles in these diseases. Estrogens are generally considered to enhance autoimmunity and have multiple effects on the immune system through various cell types and molecular pathways. There is much evidence supporting the role of estrogen in the pathogenesis of systemic lupus erythematosus (SLE): the disease occurs much more frequently in women, especially during the years of child-bearing potential, and commonly flares during pregnancy. The relationship between estrogen and the development of SLE is complex, however. Exogenous estrogens have been historically avoided in women with SLE due to the widely held view that they could activate disease and their use remains controversial. Current evidence from prospective trials suggests that there may be a small increased risk of mild/moderate flares in women with SLE taking hormone replacement therapy (HRT), but the risk of major flare does not appear to be increased. In rheumatoid arthritis, HRT does not appear to be associated with an increased risk of disease flare and may actually improve disease activity. In all individuals with autoimmune disease, the risk of venous thrombosis associated with oral HRT is an important factor that should also be considered.

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“…Reproduced with permission from Elsevier Masson [96] incidence of joint pain peaks at 50-59 years in the general population. Some preclinical studies have shown a protective effect of oestrogen in arthritis and on pro-inflammatory genes [24,25]. Clearly, there are several possible causes of arthralgia in a non-breast cancer population, which can make it difficult to elucidate one particular cause.…”

Section: Role Of Oestrogenmentioning

confidence: 99%

Aromatase inhibitor-induced arthralgia in early breast cancer: what do we know and how can we find out more?

Din

Dodwell

Wakefield

et al. 2010

Breast Cancer Res Treat

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Aromatase inhibitors (AIs) are a standard of care for the adjuvant treatment of hormone responsive early carcinoma of the breast as demonstrated in a number of large international phase III randomised trials. Arthralgia was a somewhat unexpected side effect of this class of agents and has proven to be potentially problematic in clinical practice. Although rates of up 35% have been reported in the randomised trials, the figure has been much higher in subsequent case series. There is concern that these symptoms are significant and may affect compliance and thus the overall efficacy of treatment. It is therefore extremely important that we evaluate this syndrome with a view to gaining more information regarding its clinical features and possible aetiological mechanism. The potential aetiological mechanisms and evidence for aromatase inhibitor-induced arthralgia (AIA) are reviewed in this article. Looking forward, it is now important that prospective clinical trials are well designed to evaluate this syndrome and potential therapeutic strategies to circumvent it. Radiological imaging and biochemical analyses may help our understanding of AIA and these are discussed.

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Oestrogen exhibits type II collagen protective effects and attenuates collagen-induced arthritis in rats

Cited by 37 publications

References 36 publications

Sex Differences in Autoimmune Disease from a Pathological Perspective

Sex Differences in Autoimmune Disease from a Pathological Perspective

The effects of hormone replacement therapy on autoimmune disease: rheumatoid arthritis and systemic lupus erythematosus

Aromatase inhibitor-induced arthralgia in early breast cancer: what do we know and how can we find out more?

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