Menopause and Bone Health: Hormonal Mechanisms, Osteoporosis Risk, and Management Strategies

Abstract

A decrease in estrogen levels after menopause, a normal biological transition, has a substantial effect on bone metabolism and raises the risk of osteoporosis. Reduced estrogen speeds up bone resorption, which lowers bone mineral density and increases the risk of fracture, especially in postmenopausal women. With a focus on the mechanisms driving postmenopausal osteoporosis, this article examines the physiological link between menopause and bone health. It also covers evidence-based preventive measures, such as consuming enough calcium and vitamin D, engaging in weight-bearing activity, and making lifestyle changes like quitting smoking and drinking less alcohol. Additionally, pharmaceutical treatments including selective estrogen receptor modulators, bisphosphonates, and hormone replacement therapy—are examined for their potential to prevent and treat osteoporosis. To preserve skeletal strength and lower the risk of fracture, early screening and prompt intervention are essential. In general, the development of successful preventative and therapeutic strategies to enhance the quality of life for postmenopausal women is made possible by an awareness of the multifaceted impact of menopause on bone health.

Keywords

Introduction

Menopause, which signifies the end of reproductive potential and the permanent cessation of menstruation, is a major turning point in a woman's life. It usually happens between the ages of 45 and 55 and is linked to a decrease in ovarian function, which lowers levels of progesterone and estrogen. The impact on bone health is one of the many physiological impacts of these hormonal alterations¹

By controlling the ratio of bone production to resorption, estrogen is essential for preserving bone density. Following menopause, a drop in estrogen causes an imbalance that favors bone resorption, which lowers bone mineral density and increases the risk of osteoporosis and fractures². Early prevention and treatment are crucial because osteoporosis, sometimes known as the "silent disease," advances without symptoms until a fracture happens.

The likelihood of postmenopausal bone loss is further influenced by a number of factors, such as lifestyle choices, physical activity, dietary condition, and genetic susceptibility. Developing successful preventive and treatment measures requires an understanding of these characteristics³. For postmenopausal women at risk of osteoporosis, new developments in screening, lifestyle modification, and medication therapies have improved outcomes?.

One common metabolic and non-communicable skeletal condition is osteoporosis.  Reduced bone mass and an accelerated deterioration of bone microstructure are features of this disorder?. The bone becomes brittle and more prone to breaking as a result.  This condition frequently goes undiagnosed until fractures happen, which could result in serious secondary health issues or even death?.

In order to maintain skeletal health and lessen the burden of osteoporosis among postmenopausal women, this article will examine the physiological changes linked to menopause, their effects on bone metabolism, and various preventive and therapeutic techniques.

WHAT IS MENOPAUSE

Periods permanently stop at menopause. After a year without a menstrual cycle, vaginal bleeding, or spotting, it is identified. In the 40s or 50s, menopause may occur. However, 51 is the average age?. Menopause occurs naturally.  However, menopause’s emotional and physical symptoms, such hot flashes, can interfere with sleep, reduce energy, or have an impact on mood.  There are numerous therapies, such as hormone therapy and lifestyle modifications?.

IMPACT OF MENOPAUSE ON BONE HEALTH

For women going through menopause and in the postmenopausal phase, preventing bone loss is crucial.  Menopause raises the risk of osteoporosis and dramatically accelerates bone loss.  According to research, up to 20% of bone loss may occur throughout these phases, and osteoporosis affects about 10% of women over 60 globally?.

Skeletal homeostasis depends on estrogen, which also controls bone remodeling by influencing the production of RANKL, a crucial cytokine for osteoclasts to resorb bone [3].  As a result, the osteoclast undergoes more apoptosis and less differentiation, which promotes creation.  Although the exact mechanism by which estrogen regulates the rate of bone turnover is unknown, it is known to directly affect osteoblasts, osteocytes, and a number of cytokines, including interleukin 6 ¹?.

RELATION BETWEEN ESTROGEN AND BONE HEALTH

In addition to controlling bone turnover in adult bone, estrogen is crucial for the development and maturation of bone.  For both males and females to properly close their epiphyseal growth plates during bone formation, estrogen is required.  Estrogen insufficiency increases osteoclast development and bone resorption in young skeletons as well.  Both cortical and cancellous bone loss are caused by estrogen insufficiency during menopause.  Because of penetrative resorption and microfractures, highly elevated bone resorption in cancellous bone causes overall bone loss and local architecture degradation¹¹&¹². The Initial reaction to estrogen deprivation in cortical bone is increased endocortical resorption.  Later on, intracortical porosity also rises.  These result in weakened bones, disrupted architecture, and decreased bone mass.  Estrogen inhibits osteoclast differentiation at the cellular level in bone, which lowers the number of osteoclasts and the quantity of active remodeling units¹³.  IL-1 and IL-6 are the most likely cytokines to induce this action.  Through a mechanism that is currently unknown, estrogen controls the expression of IL-6 in bone marrow cells.  It is still unclear whether estrogen directly affects osteoblasts or if the coupling phenomena between bone production and resorption is to blame¹?.

ROLE OF ENENDOCRINE IN OSTEOPOROSIS

The gradual disorder known as osteoporosis, or porous bones, causes bones to weaken structurally and become more prone to shatter or fracture.  Osteoporosis is most frequently caused by menopause.  Estrogen levels begin to fluctuate and eventually decline as hormones adjust to natural menopausal changes.  Reduced estrogen during menopause dramatically accelerates bone loss because estrogen slows the normal breakdown of bone, preventing bones from weakening¹?.

One of the three estrogen hormones that the body normally produces is estradiol.  In women going through menopause, the effects of estradiol are evident.  Women’s estradiol levels naturally decrease throughout this process because the ovaries stop producing it, which stops the monthly periods.  Mood swings, vaginal dryness, hot flashes, and night sweats—symptoms frequently linked to menopause—are sometimes brought on by this shift.  Osteoporosis may eventually result from decreased estrogen levels¹?’¹?.

Vitamin D and calcium are other hormones that play a part in bone health. Vitamin D allows your body to absorb calcium. Calcium is necessary for building strong, healthy bones. Without enough vitamin D and calcium, bones may not form properly in childhood and can lose mass, become weak, and break easily in adulthood. Even if you get enough calcium in your diet, your body will not absorb that calcium if you don’t get enough vitamin D¹?’¹?.

OSTEOPOROSIS

WHAT IS OSTEOPOROSIS

Osteoporosis is a condition of skeletal impairment due to decreased mineralized bone density (mass/unit volume). The Decreased density damages the bone strength it  leads to increased risk of fractures²?.

 CLASSIFICATION OF OSTEOPOROSIS

Osteoporosis is generally classified into primary and secondary types. Primary osteoporosis occurs without an obvious underlying disease and is further divided into three categories:

1. Postmenopausal osteoporosis (Type I): Commonly seen in women after menopause due to estrogen deficiency, leading to increased bone loss, particularly in the spine and wrist.
2. Age-related or senile osteoporosis (Type II): Gradual bone density loss associated with aging, affecting both men and women, although women are at higher risk. This type typically impacts both the spine and hip.
3. Idiopathic osteoporosis: A rare form with unknown cause, mostly observed in men and occasionally in younger adults, characterized by unexplained bone loss and fractures²¹.

Secondary osteoporosis results from identifiable medical conditions or external factors that accelerate bone loss. Common causes include chronic diseases, hormonal imbalances such as hyperthyroidism or Cushing’s syndrome (high cortisol levels), hypogonadism in men (low testosterone), prolonged use of certain medications, and lifestyle factors such as excessive alcohol consumption. This type can occur at any age and often requires treatment of the underlying condition alongside osteoporosis management²² ²³.

CLINICAL SIGNS AND SYMPTOMS OF OSTEOPOROSIS

Osteoporosis typically remains silent and shows no symptoms until a fracture occurs²?. Fragility fractures most often affect the hip, wrist, and vertebrae, and they can significantly impact quality of life by causing pain, limiting daily activities, and reducing confidence and independence. Early bone loss usually has no noticeable symptoms, but as osteoporosis progresses, individuals may develop back pain from vertebral compression, gradual loss of height, a stooped posture, or fractures that occur with minimal trauma²?.

RISK FACTORS OF OSTEOPOROSIS

A poor diet and lack of physical activity can increase the risk of chronic diseases like osteoporosis. Eating nutritious foods rich in protein, calcium, vitamin D, fruits, and vegetables helps maintain strong bones, while high-calorie diets and alcohol weaken them. Studies, show that inactivity lowers bone mineral density. Calcium is essential for bone growth, but the body needs enough vitamin D to absorb it properly. Low sunlight exposure, poor diet, and high caffeine intake can all reduce calcium availability, increasing the risk of weak bones²? ²?.

Alcohol consumption even at low or moderate levels negatively affects bone health in both men and women, reducing bone density in key areas of the skeleton. Alcohol directly harms bone cells by slowing their growth and activity, and heavy drinking worsens this through poor nutrition, low calcium intake, reduced mobility, and vitamin D deficiency. Smoking is another major risk factor for osteoporosis, as it leads to lower bone mass and a higher risk of fractures. This is largely due to its impact on estrogen, where smokers experience reduced hormone levels and faster clearance, contributing to earlier menopause and accelerated bone loss in women. In men, smoking is also associated with decreased bone mineral density²? ²?.

Reproductive factors such as oral contraceptive use, late menarche, irregular menstrual cycles, breastfeeding and periods of amenorrhea can contribute to reduced bone mineral density in women. Those who start menstruation later often develop lower peak bone mass and have a higher fracture risk. Studies also show that women with menstrual irregularities like oligomenorrhea or amenorrhea generally have lower BMD than healthy controls²?.

Genetics plays a major role in osteoporosis. Our genes strongly influence peak bone mass, where their impact is most significant. They may also affect fracture risk in ways that go beyond just bone mineral density²? ²?.

Rheumatoid arthritis (RA) is a common inflammatory disease in adults, and its ongoing inflammation, reduced mobility, and frequent use of glucocorticoids all contribute to osteoporosis. RA causes two types of bone loss: a generalized form that affects major areas like the spine, pelvis, hips, ribs, and upper arms, and a localised form around joints that are actively inflamed. Research shows that people with RA have a higher risk of spine and hip fractures than those with primary osteoporosis. This generalized bone loss is driven by reduced bone formation and increased bone breakdown, as seen in studies²?.

Medications like synthetic glucocorticoids are treated for various disease conditions. They are the leading cause of secondary osteoporosis. Glucocorticoids increase bone breakdown by raising RANKL levels and lowering its protective counterpart, OPG. They also suppress IGF-1 activity, reducing bone formation and collagen production, which further weakens the skeleton²? ²?.

TREATMENT OF OSTEOPOROSIS

The main goal in managing osteoporosis is to prevent fractures, slow down bone weakening, and reduce long-term disability. Prevention involves minimizing fall risks, improving vision or hearing, limiting alcohol and smoking, and maintaining good nutrition with enough calcium, vitamin D, and protein²?. Treatment is advised for people with previous hip or spine fractures, very low bone density, or those whose FRAX score indicates a high 10-year fracture risk. Studies show that the strongest benefits of therapy occur in individuals with severe low bone density or a history of major fractures²? ³?.

PHARMACOLOGICAL TREATMENT

Bisphosphonates are first-line drugs for osteoporosis because they slow bone breakdown by inhibiting osteoclasts. Oral options like alendronate and risedronate lower both vertebral and hip fracture risk, while ibandronate mainly reduces spine fractures. They must be taken on an empty stomach with water, and the patient should stay upright for at least 30 minutes to avoid GI irritation and improve absorption. Injectable forms such as zoledronic acid and IV ibandronate are helpful for high-risk patients who cannot tolerate oral therapy. These drugs bind to bone minerals, reduce bone turnover, and work best when vitamin D levels are adequate ²? ²? ³?.

Raloxifene is a selective estrogen receptor modulator used mainly for postmenopausal women with osteoporosis, and it is effective primarily in reducing vertebral fractures. It acts like estrogen on bones to slow bone loss but blocks estrogen activity in breast and uterine tissue, which also lowers the risk of invasive breast cancer. It may worsen hot flashes and increases the risk of venous thromboembolism, so it’s suitable only for women without VTE risk or vasomotor symptoms and who cannot take bisphosphonates. AACE recommends it mainly for patients who only need spine-fracture protection. The standard dose is 60 mg daily, but it should be avoided in pregnancy, breastfeeding, and in women with a current or past VTE history ²? ³¹.

Calcitonin nasal spray is an antiresorptive option for postmenopausal osteoporosis, but it mainly reduces spinal fractures and is less effective than other first-line treatments. It can help relieve pain from acute or chronic vertebral compression fractures, though concerns about a possible cancer risk limit its use. Calcitonin slows bone resorption and modestly increases bone density, mostly in the spine. It is available as a nasal spray or injectable form ²? ²?.

Teriparatide is an anabolic (bone-building) form of recombinant parathyroid hormone that directly stimulates osteoblasts to form new bone. Given as a daily 20 mcg subcutaneous injection for up to two years, it effectively lowers both vertebral and non-vertebral fracture risk. It is mainly used for severe osteoporosis, high-risk patients, or those who do not respond to bisphosphonates. Teriparatide is often considered when conventional antiresorptive treatments fail²? ²?.

Denosumab is a monoclonal antibody that inhibits osteoclast activity, helping increase bone density and reduce hip, spine, and other fractures. A 60 mg injection every six months has shown greater BMD gains than weekly alendronate and is useful when bisphosphonates fail. It can be used cautiously in patients with mild to moderate kidney disease²?.

Estrogen therapy, with or without progesterone, can modestly reduce hip and spine fractures, but the increased risks of stroke, VTE, heart disease, and breast cancer limit its use. Lower-dose estrogen can improve bone density, though its long-term safety and fracture-prevention benefit remain uncertain. While estrogen helps slow bone turnover and preserve bone mass especially when combined with calcium it is not recommended as a first-line long-term treatment for osteoporosis in women over 50. HRT works best when started early in menopause but bone loss can accelerate once the therapy is discontinued²? ²?.

Combination therapy for osteoporosis hasn’t shown clear fracture-reduction benefits and is mostly limited to research settings. Although pairing anabolic and antiresorptive drugs can boost bone density more than using one alone, evidence is still insufficient. Various small trials have tested PTH-based therapies with agents like estrogen, raloxifene, bisphosphonates, and denosumab, but routine use is not recommended ²? ³².

NON-PHARMACOLOGICAL TREATMENT

Hip fractures are a serious consequence of osteoporosis, particularly in elderly individuals prone to falls. Hip protectors, made of polypropylene or polyethylene shells, help absorb the impact of falls and redirect stress to surrounding soft tissue, lowering fracture risk. Vertebral compression fractures can lead to severe spinal deformity, chronic pain, and reduced quality of life. While initial management includes rest, pain relief, and bracing, persistent or severe cases may require minimally invasive procedures like vertebroplasty—injecting bone cement into the vertebra—or balloon kyphoplasty, which also aims to restore vertebral height and correct spinal curvature. Both procedures are guided by fluoroscopy to ensure precision and safety³³.

Non-drug approaches to support bone health include calcium and vitamin D supplementation, weight-bearing and resistance exercises, muscle-strengthening activities, and measures to prevent falls.

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