How does hrt help osteoporosis

For symptomatic menopausal women with hot flashes and bone loss who have undergone a hysterectomy, use HT with estrogen. To prevent osteoporosis in women with a uterus under age 65, I urge doctors to prescribe estrogen-progesterone therapy. Five to 15 percent or more of women on HT can still lose bone density. This means that women on HT need to be monitored with periodic bone densitometry.

Parathyroid hormone, serum protein electrophoresis, gluten celiac testing, hour cortisol levels, and fasting urine NTX N-terminal telopeptide testing also can be useful.

The bottom line is that hormone therapy can be considered for bone health — in particular with concomitant menopausal symptoms that could be improved.

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Our Research Strategy. Research Roadmap. Women up to the age of 60 who use HRT for relief of menopausal symptoms can be reassured that benefits of HRT will exceed risk, and the potential bone protective effect will be an additional benefit. It is hoped that these recommendations will be widely accepted so that once again, HRT can be used appropriately to give women the bone protection that they require.

Menopause International ; The key recommendations are summarised as follows: The decision to take HRT should be made after full discussion and consideration of risks and benefits, with regular review.

The effect did not differ in women stratified by BMI, age, time since menopause [ 21 ]. The WHI is the first randomized trial with definitive data supporting the ability of postmenopausal HRT at standard doses to prevent fractures at the hip, vertebrae, and other sites.

The WHI findings are particularly relevant since the study subjects were not specifically selected on the basis of a high risk of osteoporosis and related fracture or a known history of osteoporosis with or without prior fracture.

Thus, standard HRT is effective in preventing bone loss associated with the menopause and decreases the incidence of all osteoporosis-related fractures, including vertebral and hip fractures, even in women not selected for a high fracture risk. Based on evidence of effectiveness, cost and safety, standard HRT should be considered one of the first-line therapies for the prevention and treatment of fractures in postmenopausal women, younger than 60 years [ 24 , 25 ].

Conversely, according to the available evidence, the initiation after the age of 60 years of HRT for the sole purpose of fracture prevention is not recommended.

In women that are already on HRT, the continuation of HRT after the age of 60 years should take into account the possible long-term effects of the specific dose and method of administration of HRT, compared to other proven non-hormonal therapies [ 24 , 25 ]. Many women drop out of the standard dose HRT because of the side effects, and bone sparing effect can be lost a few years after discontinuation [ 26 ].

The strategy to maintain the beneficial estrogen effect on bone is to improve long-term compliance and continuation reducing the HRT dosage. The usually prescribed HRT dosage has declined progressively over the past 20 years [ 24 , 27 — 30 ].

The use of low and ultra low dose of estrogen has grown in popularity Table III. In addition, the HOPE trial demonstrated the beneficial effects of these low-dose regimens on vasomotor symptoms and vaginal atrophy, lipid profiles, bleeding profiles, and endometrial hyperplasia [ 29 ].

Thus, LD-HRT may enhance patient continuation, with adequate bone protection and menopausal symptom control. LD-HRT gives physicians the possibility to personalize the doses on the basis of each individual patient's needs. In addition, ultra-low dose estrogen could be appropriate as a new start for women aged 60 and older, who might benefit from modest increases in estrogenic action sufficient for their age to preserve skeletal integrity, possibly without significant breast effects and endometrial stimulation.

Osteoarthritis OA is an aging-related chronic joint disease. The social and economic impact of the disease is tremendous as OA is the major reason for disability and reduced quality of life among older people [ 31 ]. Preclinical studies demonstrate that estrogen decline can have a major effect not only in the pathogenesis of osteoporosis but also of OA [ 32 , 33 ].

Such an effect is prevented and in some cases reversed with estrogen therapy [ 33 ]. The marked predominance of polyarticular osteoarthritis in women and, in particular, the marked increase in osteoarthritis in women after the menopause both point to a likely involvement of female sex steroids in the maintenance of cartilage homeostasis. Estrogen receptors have been identified in the intervertebral disk and estrogen has a protective, mitogenic effect [ 34 ].

Apart from its positive effect on the bone, it has been recently found that estrogen induces favorable changes in the intervertebral discs. After menopause, intervertebral disk space shows a progressive decrease that almost entirely occurs in the first years since menopause, suggesting that the estrogen decrease may rapidly change connective tissue metabolism in the intervertebral disks [ 35 ].

Estrogen decline after menopause leads to changes in the connective tissue matrix and estrogen therapy may prevent and at least in part reverse these changes [ 36 ]. These effects are relevant since disc space narrowing is a clear risk factor for vertebral fracture. In addition, the stimulation of estrogen receptor by estrogen and a selective estrogen receptor modulator SERM may protect postmenopausal women from an excessive cartilage turnover [ 37 ].

Tibolone is a synthetic steroid, a norethisterone de-rivative, metabolized to molecules that have affinity for the estrogen, progesterone and androgen receptors, which has been described as a selective estrogenic activity regulator STEAR.

Different tibolone doses resulted in a suppression of bone turnover and long-term positive effects on bone mineral density measured at different skeletal sites [ 38 ]. A low dose of 1.

In this study, tibolone was associated with an increased risk of stroke. This deleterious effect on stroke risk must be ascribed to the age of the population treated. In fact, in all studies in which the standard dose of tibolone was used, no increased risk of stroke was reported [ 24 ]. In addition, the low-dose tibolone used in the LIFT study was associated in a reduced risk of endometrial, colon and breast cancer, and no increase in the risk of venous thromboembolism was seen [ 39 ].

The concerns on long-term use of estrogens have focused the attention on strategies to reduce the possible impact of estrogen on the breast cancer risk. The selective estrogen modulators SERMs are chemically different compounds that lack the steroid structure of estrogens, but are able to interact with estrogen receptors as agonists or antagonists depending on the target tissue.

The early SERMs, tamoxifen and raloxifene were originally developed for the prevention and treatment of breast cancer and were subsequently found to conserve bone mass. Tamoxifen has been used for over 30 years, either as adjuvant treatment of, and also to prevent breast cancer incidence in high-risk women. Tamoxifen showed a significant bone sparing effect [ 40 ], but its use was linked with increased risks of endometrial cancer, stroke, pulmonary emboli, deep-vein thrombosis, and cataracts, and thus it is not indicated for the prevention or treatment of postmenopausal osteoporosis.

Raloxifene is the first SERM approved for the treatment and prevention of osteoporosis in postmenopausal women in the United States and Europe. A third-generation SERM, bazedoxifene was extensively evaluated in preclinical studies producing convincing data supporting its use as an antiresorptive agent for the prevention and treatment of postmenopausal osteoporosis. Bazedoxifene reduces bone turnover and maintains or increases vertebral and femoral BMDs in comparison to placebo [ 43 ].

In a 3-year RCT, placebo- and active-controlled trial of 7, women, bazedoxifene reduced the risk for new vertebral and non-vertebral fractures in high-risk women [ 44 ]. Bazedoxifene is safe and well tolerated, with no evidence of endometrial or breast stimulation. These data suggest that bazedoxifene may offer significant clinical benefits for postmenopausal women with or at risk of osteoporosis. A new goal in preventing postmenopausal osteoporosis is the combination of a SERM with an estrogen, in order to treat climacteric syndrome, preventing the bone consequences of estrogen decline, and in the meantime, avoiding the use of progestogens.

This novel approach has been evaluated with bazedoxifene which could yield the beneficial effects of estrogens and SERMS, while potentially being more tolerable and safer than standard HRT, avoiding the potential deleterious effects of synthetic progestins [ 24 ]. Postmenopausal osteoporosis and related fractures is a serious health threat that can affect nearly half of all white women over the age of 50, and about half of elderly women will have long-term disability, morbidity and death after a fracture.

This advice was based mainly on the presentation and interpretation of the WHI data that were greatly revised by the menopause community [ 24 , 25 ]. Years ago we forecasted that the drop in HRT use could have caused an increase in fragility fractures in elderly women [ 46 ]. In a recent study, Karim et al. In this huge cohort of postmenopausal women followed for 6. This study evaluated the incidence of hip fractures and did not analyze the effect of HRT discontinuation on other fractures, such as vertebral or wrist fractures.

However, we can assume that the burden of HRT withdrawal, particularly on different skeletal sites, such as vertebral bodies where trabecular bone is prevalent, will be far more substantial. Thus, the Karim study results [ 48 ] perhaps even underestimated the overall effect of HRT discontinuation on postmenopausal bone health.

This important study cannot be ignored or disregarded by health-care providers and, most importantly, by Regulatory Agencies worldwide. Today there is an urgent need to identify new approaches for long-term osteoporosis prevention.

Nevertheless, and in the meantime, the current view and recommendations from Regulatory Agencies about HRT need to be revisited and revised without delay. The use of HRT for osteoporosis prevention is based on biology, epidemiology, animal and preclinical data, observational studies and randomized, clinical trials, and thus bone protection has been included among the benefits of HRT in recent recommendations [ 24 , 25 ].

In fact, osteoporosis prevention can actually be considered as a major additional effect in perimenopausal women who use HRT for treatment of climacteric symptoms. Appropriate and effective HRT dose and regimen need to be individualized. There is no evidence that alternative treatments to HRT in early postmenopausal period are also beneficial, not only for symptoms but also for osteoporosis prevention.

Individual risk-benefit considerations remain subjects for discussions between individual patients and their care-givers. The possibility that LD-HRT or TSEC decrease the fracture risk is not demonstrated but data on bone turnover and density in early postmenopausal women are indicating a strong protective effect and the rationale for future well-conducted prospective studies. National Center for Biotechnology Information , U.