Menopause, Bone Health, And Intimate Wellness – What Estrogen Decline Can Affect

Introduction 

The decline in estrogen during menopause can be associated with changes in multiple body systems because estrogen receptors are found in many tissues throughout the body, including bone and genitourinary tissues. Although estrogen is often recognized primarily as a reproductive hormone, its role extends beyond reproduction. Fuentes and Silveyra explain that estrogen receptor signaling can work differently depending on the tissue involved. In other words, estrogen may send different cellular signals in different parts of the body. This helps explain why estrogen decline can affect more than menstrual cycles or fertility. Amongst other areas, estrogen decline can meaningfully affect skeletal and genitourinary health influencing long-term bone strength, physical comfort, sexual well-being, urinary function, and overall quality of life.⁶^,²⁵ 

Perimenopause means “around menopause.” It is the transition period leading up to menopause, when the ovaries gradually produce less estrogen and hormone levels begin to fluctuate. During this stage, a woman may still have menstrual periods, but cycles often become less predictable. Periods may become heavier, lighter, closer together, farther apart, or skipped.¹³ 

Over time, these hormonal changes lead to menopause. Menopause is the permanent cessation of menstrual cycles resulting from the loss of ovarian follicular activity and is clinically recognized after 12 consecutive months without menstruation. This transition is marked by a substantial decline in ovarian estradiol production. Estradiol is the main and most potent form of estrogen during the reproductive years.¹³ 

During perimenopause, menopause, and especially postmenopause, lower estrogen levels can cause vaginal and vulvar tissues, as well as lower urinary tract tissues such as the urethra and bladder, to become thinner, drier, less elastic, more fragile, and more easily irritated. These changes can contribute to symptoms such as vaginal dryness, irritation, urinary urgency, urinary frequency, recurrent urinary tract infections, and painful intercourse. This collection of symptoms is often called genitourinary syndrome of menopause, or GSM.²⁵ GSM can affect quality of life in several interconnected ways. Symptoms may influence how a woman moves through daily life, how comfortable she feels in her body, how confident she feels, how well she sleeps, the activities she chooses, and how she experiences intimacy and relationships.²³ 

This literature review examines how declining estrogen affects women’s bone health and contributes to GSM. It also considers the role of nutrition and lifestyle strategies that may support health during and after the menopausal transition. The information presented is for educational purposes only and is not intended to replace the advice, diagnosis, or treatment recommendations of a qualified medical professional. 

Effects of Estrogen Decline on Bone Health 

Estrogen is a major hormonal regulator of bone metabolism, the process by which the body maintains, breaks down, and repairs bone tissue. Bone is not static; it is living tissue that is continually remodeled throughout life. This remodeling depends largely on two types of bone cells: osteoclasts, which break down and remove old or weakened bone through bone resorption, and osteoblasts, which build new bone through bone formation.^16,17 

Estrogen helps regulate this process by limiting excessive bone resorption (breakdown and removal of bone tissue) and supporting the balance between bone breakdown and bone formation. After menopause, estrogen levels decline substantially. As a result, bone resorption may increase, and bone formation may not keep pace. When bone is broken down faster than it is rebuilt, bone mineral density decreases. This loss includes reduced mineral content, primarily calcium and phosphate in the form of hydroxyapatite, which helps give bone its hardness and strength.^16,29 

Menopause-related bone loss can affect both cortical bone, the dense outer layer of bone, and trabecular bone, the porous, honeycomb-like bone found inside areas such as the spine, hip, and ends of long bones. Because trabecular bone is remodeled more frequently than cortical bone, it may be affected earlier and more rapidly by estrogen decline. Over time, this imbalance can make bone more porous and structurally weaker, contributing to osteopenia and, if bone loss progresses, osteoporosis. Osteoporosis increases fracture risk because weakened bone is less able to tolerate everyday stress or sudden impact, such as from a fall.^29,32 

Because estrogen decline can accelerate bone loss, lifestyle, nutrition, and safety measures that help protect bone health are especially important during and after the menopausal transition.^16,32 

Nutrition and Lifestyle Considerations for Bone Health 

Calcium and Vitamin D 

Calcium is a major mineral in bone, and adequate intake helps maintain bone structure and strength. Vitamin D supports bone health by helping the body absorb calcium from the digestive tract and by contributing to bone mineralization.^14,24 The body closely regulates blood calcium because calcium is essential for muscle contraction, nerve signaling, and heart rhythm. When calcium intake is insufficient, or when vitamin D levels are too low to support calcium absorption, the body may pull calcium from bone stores to help keep blood calcium within a normal range.^14,24 For this reason, a normal blood calcium level does not necessarily mean that calcium intake or long-term bone stores are adequate. Calcium adequacy is better assessed by considering usual dietary intake, vitamin D status, kidney function, medications, fracture risk, and, when appropriate, bone density testing. Clinicians may also evaluate related markers, such as 25-hydroxyvitamin D and parathyroid hormone, based on individual risk factors.^5,21 

Current evidence suggests that calcium and vitamin D intake may be most important when dietary intake or vitamin D status is insufficient, rather than as a blanket intervention for all postmenopausal adults.²⁸ 

Protein 

Bone is not made of minerals alone. It also contains a collagen-based protein matrix that provides structure and flexibility. Adequate protein intake is important for bone health because protein supports the collagen framework of bone, tissue repair, muscle strength, balance, and mobility.^7,30 By helping maintain muscle mass, adequate protein intake may also support strength, stability, and fall-risk reduction.^7,30 

Adequate total protein intake, sufficient calcium and vitamin D, and regular resistance and weight-bearing exercise work together to support bone and muscle health. Protein can come from a variety of foods, including dairy, fish, eggs, lean meats, soy, legumes, nuts, and seeds, as part of a balanced diet.^7,30 

Resistance Training 

Resistance training includes exercises in which muscles work against force, such as lifting weights, using resistance bands, performing body-weight exercises, squats, lunges, or using strength machines. When muscles contract during resistance training, they pull on bones through the tendons. This creates stress, tension, and small bending forces on the skeleton. Bone cells can sense this mechanical strain and respond by signaling the body to maintain or build bone tissue.^2,12 

The key mechanism involves osteocytes, mature bone cells embedded within bone tissue that act as mechanical sensors. When osteocytes detect stress from lifting, pushing, pulling, squatting, or other resistance exercises, they help regulate bone remodeling by influencing osteoblasts, which build bone, and osteoclasts, which break bone down.^2,12 

Resistance training may help shift bone remodeling in a healthier direction by supporting bone formation and limiting excessive bone breakdown. It also strengthens the muscles around the skeleton, improving balance, stability, posture, and fall protection. This matters because fracture risk is not only related to bone density; it is also related to the likelihood of falling.^11,12 

Weight-Bearing Exercise 

Weight-bearing exercise refers to activities performed while standing, in which the bones and muscles work against gravity to support the body. Examples include walking, stair climbing, dancing, jogging, and hiking. These activities place force through the skeleton, signaling that the bones need to remain strong.^2,12 

In simple terms, weight-bearing exercise tells the skeleton: “This bone is needed, so keep it strong.” Bones respond to regular loading and impact by maintaining, and in some cases improving, their density and strength.^2,12 

As with resistance training, the main mechanism involves osteocytes. During weight-bearing activity, the force of body weight and ground impact travels through the bones. Osteocytes detect this strain and help regulate bone remodeling by signaling osteoblasts to build bone and osteoclasts to remove old or damaged bone in a controlled way.^2,12 

Weight-bearing exercise is especially helpful because it places repeated, healthy stress on bones in areas commonly affected by bone loss, including the hips, spine, legs, and feet. Over time, regular weight-bearing activity can help preserve bone mineral density, support bone strength, and improve mobility and balance, which may reduce the risk of falls and fractures.^11,12 

Fall Prevention 

Fall prevention is an important part of bone-health care because many osteoporotic fractures occur after a fall. Osteoporosis makes bones less dense, weaker, and more fragile, reducing their ability to tolerate sudden impact. A fall that might only cause a bruise in someone with stronger bones can lead to a fracture in someone with osteoporosis, especially in areas such as the hip, wrist, spine, shoulder, and pelvis.^11,31 

Bone strength is not determined by bone mineral density alone. It also depends on bone quality, including the internal architecture of the bone. In osteoporosis, the inner “scaffolding” becomes thinner and more porous, making bone less able to absorb shock and distribute force when a person lands.³¹ 

Falls are especially concerning because they combine several fracture risks at once: sudden impact, body-weight force, awkward landing position, and sometimes twisting. For example, falling sideways onto the hip can send a large amount of force through the femur and hip joint. If the bone is already weakened, that force may be enough to cause a fracture.^11,31 

For this reason, osteoporosis prevention should include both bone-strengthening strategies and fall-prevention measures, such as improving balance, addressing muscle weakness or gait instability, correcting vision problems, wearing supportive shoes, keeping floors clear, using good lighting, installing grab bars, and reviewing medications that may cause dizziness or sedation.¹¹ 

Limiting Smoking 

Smoking is harmful to bone health because it is associated with lower bone mineral density, poorer blood flow, impaired bone healing, and increased fracture risk. It may also affect hormones and inflammation in ways that worsen skeletal health. Avoiding smoking is recommended because tobacco use is linked with reduced bone density, impaired bone repair, and higher fracture risk.³⁶ 

Limiting Excessive Alcohol 

Heavy alcohol use can interfere with calcium and vitamin D metabolism, impair bone-forming cells, increase the likelihood of falls, and contribute to poor nutrition. Limiting excessive alcohol intake may help protect bone health by supporting normal bone metabolism, preserving balance and coordination, and reducing the likelihood of fall-related fractures.^18,35 

Metabolic Health, Nutrient Status, and Body Composition 

Bones do not function in isolation. Skeletal health is closely connected to metabolic health, nutrient status, and body composition. Metabolic health describes how well the body regulates blood sugar, inflammation, cardiovascular function, hormone balance, and other processes that influence how nutrients are used throughout the body. Nutrient status describes whether the body has enough vitamins, minerals, protein, and other building blocks to support normal function, including the maintenance of strong bones and muscles. Working together, metabolic health and nutrient status influence the body’s absorption, transport, use, and storage of the dietary materials needed for bone remodeling, muscle function, balance, and mobility.^5,14,22,24 

Body composition is a part of this picture because it includes fat mass, muscle, bone, water, and other lean tissue. Fat mass can influence inflammation and hormone activity; muscle helps stimulate and support bone while also supporting strength, balance, and mobility; bone reflects skeletal structure and mineral stores.^4,5,35 Water is an important component of lean body mass that supports normal physiological functions, including circulation, temperature regulation, nutrient transport, joint lubrication, and muscle function. For skeletal health, relevant metabolic markers may include vitamin D, calcium, parathyroid hormone, kidney function, thyroid-related labs, blood glucose or hemoglobin A1c, and inflammatory markers such as C-reactive protein.^14,22,24 

When the body is not well nourished, not moving enough, inflamed, or struggling to manage blood sugar or weight-related health issues, bones and muscles may not stay as strong. This can make it harder to move safely and may increase the risk of falls and fractures.^22,24,35 

Does Body Weight Matter? 

People with higher body weight may sometimes have higher bone mineral density because added weight places more load on the skeleton, and bones can respond to repeated weight-bearing demand by becoming denser. Body weight alone, however, does not tell the whole story of skeletal health. Bone strength also depends on bone quality, muscle strength, balance, mobility, inflammation, blood sugar regulation, hormone activity, and nutrient absorption. When excess body fat is accompanied by inflammation, poor glucose regulation, reduced mobility, or low muscle strength, the added weight may place stress on the body without fully protecting the bones. For this reason, contrary to popular belief, obesity does not necessarily protect against fracture, even when bone mineral density appears higher.³⁵ 

Body weight below an optimal range can also be a concern for skeletal health, particularly when it is accompanied by low muscle mass, inadequate calorie or protein intake, nutrient deficiencies, hormonal disruption, or frailty. Lower body weight places less mechanical load on the skeleton, while low muscle mass can affect strength, balance, and fall risk. 

Body weight matters but it is one of many determinants of bone health. Bone density, bone quality, nutrition, mobility, medication use, hormone status, and fracture history are integral components of bone health.^5,15 As a whole, nutrition and lifestyle strategies can play an important supportive role during and after the menopausal transition. Adequate calcium, vitamin D, and protein intake; regular resistance and weight-bearing exercise; fall prevention; avoidance of smoking; moderation of alcohol intake; and attention to metabolic health may help preserve bone strength, mobility, balance, and overall function.^5,14,34 These strategies are supportive rather than curative. They may help reduce risk, preserve function, and support bone strength, but they do not fully reverse estrogen-related skeletal changes when medical treatment is indicated.^24,34 

Estrogen Decline and Genitourinary Syndrome of Menopause (GSM) 

How Lower Estrogen Affects Vaginal and Vulvar Tissues 

In addition to its role in skeletal remodeling, estrogen also helps maintain the structure and function of genitourinary tissues, making GSM another important consequence of the post-menopausal low-estrogen state. Estrogen helps maintain the thickness, moisture, elasticity, blood flow, and resilience of vaginal and vulvar tissues. Under adequate estrogen influence, the vaginal lining is typically thicker, better lubricated, and more flexible. Estrogen also supports glycogen production in vaginal epithelial cells. Glycogen helps nourish lactobacilli, beneficial bacteria that support a more acidic vaginal environment.^19,25 

When estrogen declines during and after menopause, the vaginal lining may become thinner, drier, less elastic, and more easily irritated. These tissue changes help explain why some women experience vaginal dryness, burning, itching, soreness, decreased lubrication, or pain with intercourse.^10,25 In plain language, estrogen helps keep vaginal tissue “plump,” moist, flexible, and resilient; when estrogen decreases, the tissue may become more delicate, dry, and prone to discomfort. 

How Lower Estrogen Affects Urinary Tissues 

The urinary tract is also estrogen-sensitive. The urethra and bladder contain estrogen receptors, and estrogen helps maintain the health of the urethral lining, surrounding connective tissue, blood flow, and local microbial environment.^10,25 With lower estrogen, urethral and bladder tissues may become more vulnerable to irritation. Changes in vaginal pH and the microbiome may also allow harmful bacteria to grow more easily, increasing susceptibility to recurrent urinary tract infections in some postmenopausal women.^3,27 

These changes may also contribute to urinary urgency, frequency, discomfort with urination, or increased urinary symptoms even when no infection is present.^10,25 

Common GSM-Related Symptoms 

GSM can involve overlapping vaginal, vulvar, sexual, and urinary symptoms. Table 1 organizes common symptoms by affected area to show how estrogen-related tissue changes may appear in different but connected parts of the genitourinary system. 

Table 1. Common Symptoms Associated With Genitourinary Syndrome of Menopause 

Area Affected	Possible Symptoms
Vaginal/Vulvar Tissues	Dryness, burning, itching, irritation, soreness, decreased lubrication
Sexual Comfort/Function	Pain with intercourse, bleeding or spotting after intercourse, reduced comfort, avoidance of sex due to discomfort
Urinary Tract	Urgency, frequency, discomfort with urination, recurrent urinary tract infections

GSM is not limited to vaginal dryness alone; it can affect physical comfort, sexual function, urinary health, and daily well-being.²³ 

These symptoms are common, but they are not something women simply have to tolerate. GSM provides a useful clinical framework for understanding how estrogen decline affects both genital and urinary tissues.²⁵ GSM symptoms may persist or progress without treatment because the underlying tissue changes are related to the sustained low-estrogen state of postmenopause.^10,25 Recognizing GSM is important because symptoms such as vaginal dryness, dyspareunia (persistent or recurrent genital pain that occurs just before–because the body begins to anticipate pain, during, or after sexual intercourse), urinary urgency, and recurrent urinary tract infections can significantly affect comfort, sexual function, quality of life, and daily well-being.^10,25,26 In the context of GSM, quality of life may include physical comfort, urinary control, sexual comfort, emotional well-being, sleep, relationships, and participation in daily activities. 

Treatment Options and Symptom-Based Care 

The evidence generally supports a stepwise, symptom-based approach to GSM. Mild symptoms may improve with non-hormonal vaginal moisturizers and lubricants, while persistent or moderate-to-severe symptoms often respond best to local vaginal estrogen or other prescription vaginal therapies.^10,26,33 

Local vaginal estrogen is placed directly in the vagina, usually as a cream, tablet, insert, or ring. Unlike systemic estrogen, which is taken orally or through a skin patch and circulates through the bloodstream to affect estrogen-sensitive tissues throughout the body, local vaginal estrogen delivers low-dose estrogen directly to estrogen-sensitive tissues of the vulva, vagina, urethra, and bladder, with primarily local tissue-level effects.²³ Its purpose is to treat estrogen-sensitive tissues in the vulva, vagina, urethra, and bladder with low-dose estrogen exposure at the tissue level. Local vaginal estrogen works by improving maturation and thickness of the vaginal epithelium, increasing lubrication, lowering vaginal pH, and supporting a healthier vaginal microbiome.^10,26,33 It may also help some urinary symptoms, especially recurrent urinary tract infections in postmenopausal women. Evidence suggests that vaginal estrogen can reduce recurrent UTIs by improving the vaginal environment and reducing colonization with uropathogenic bacteria.²⁷ 

Vaginal moisturizers are non-hormonal products used regularly, not only during sexual activity. They are intended to hydrate vaginal tissues and reduce dryness and irritation. Moisturizers may help mild GSM symptoms and may be especially useful for women who cannot or do not want to use estrogen. However, they do not reverse estrogen-related tissue changes in the same way vaginal estrogen can. They may improve comfort, but they generally do not restore vaginal epithelial thickness, elasticity, or pH as effectively as estrogen-based therapies.^10,26,33 

Lubricants are used during sexual activity to reduce friction and discomfort. They may be water-based, silicone-based, or oil-based. Lubricants can improve sexual comfort when dryness contributes to pain with intercourse, but their effect is temporary. Unlike moisturizers, they are not intended to provide ongoing tissue hydration, and unlike vaginal estrogen, they do not treat the underlying estrogen-related thinning of vaginal tissues.^10,26 

Pelvic floor physical therapy may be helpful when GSM symptoms overlap with pelvic floor muscle tension, urinary urgency, urinary frequency, pelvic pain, painful intercourse, or difficulty relaxing during penetration. Current GSM guidance recognizes that treatment should be individualized and may include both tissue-directed therapies, such as local vaginal estrogen when appropriate, and supportive approaches that address pain, urinary symptoms, and sexual function.^19,23 Pelvic floor therapy does not replace estrogen’s effect on vaginal tissue, but it can address muscular and functional contributors to pain and urinary symptoms.^8,20 

For example, a woman may have vaginal dryness from estrogen decline and also develop pelvic floor guarding because intercourse has become painful. In that case, local estrogen may improve tissue quality, while pelvic floor therapy may help reduce muscle tightness, improve coordination, and restore comfort. Pelvic floor therapy is best understood as a complementary treatment rather than a direct substitute for estrogen-based tissue restoration.^8,20 

The treatment options for GSM differ in purpose, strength, and limitations. Table 2 summarizes these options to clarify which treatments provide temporary symptom relief, which address estrogen-related tissue changes more directly, and which may help with muscular or functional symptoms. 

Table 2. Comparison of Common Treatment Options for Genitourinary Syndrome of Menopause 

Treatment	Main Role	Strengths	Limitations
Lubricants	Used during sex	Immediate reduction in friction and discomfort	Temporary; does not treat underlying tissue changes
Moisturizers	Used regularly	Non-hormonal relief of dryness and irritation	May be less effective than estrogen for moderate-to-severe GSM
Local vaginal estrogen	Direct treatment of vaginal and urinary tissues	Strong evidence for GSM; low systemic exposure	Requires medical review, especially with certain cancer histories
Pelvic floor therapy	Addresses muscular and functional urinary or sexual pain symptoms	May help urinary symptoms, pelvic pain, dyspareunia, and muscle guarding	Does not directly restore estrogen-depleted tissue

This comparison shows that GSM care is often symptom-based rather than one-size-fits-all. Lubricants and moisturizers may improve comfort, while local vaginal estrogen more directly treats estrogen-related tissue changes. Pelvic floor therapy may be useful when pain or urinary symptoms involve muscle tension, coordination, or guarding.^20,23 

Conclusion 

Estrogen decline is a normal part of the menopausal transition. Because estrogen receptors are located throughout the body, lower estrogen can affect health beyond the reproductive system, including measurable effects on bone strength and genitourinary health.^16,25 

Nutrition and lifestyle strategies are important for preserving bone health during and after the menopausal transition. These strategies include adequate calcium and vitamin D intake, sufficient protein consumption, resistance training, weight-bearing exercise, fall prevention, avoidance of smoking, moderation of alcohol intake, and attention to overall metabolic health.^30,37 Although these approaches do not replace estrogen’s direct role in bone remodeling, they support bone mineralization, muscle strength, balance, mobility, and fracture prevention.^12,37 

GSM can also affect quality of life in meaningful ways, including physical comfort, urinary health, sexual well-being, emotional wellness, relationships, and daily functioning.^10,25 Because the body functions as an interconnected system, habits that support overall health may also support quality of life during the menopausal transition and beyond. While nutrition and lifestyle strategies do not replace medical evaluation or treatment when needed, women may consider practices known to contribute to well-being, including balanced nutrition, regular physical activity, limiting smoking and excessive alcohol use, and managing metabolic health.^12,37 

Ultimately, bone health and genitourinary health should be understood within the broader context of whole-body wellness. Women experiencing menopausal symptoms or concerns about bone loss should consult with a qualified medical professional to discuss individualized recommendations, appropriate screening, and treatment options. At the same time, adopting health-supportive nutrition and lifestyle practices may help women maintain strength, mobility, comfort, and overall quality of life.^10,25,37 

References 

1. Armstrong LE, Johnson EC. Water intake, water balance, and the elusive daily water requirement. Nutrients. 2018;10(12):1928. doi:10.3390/nu10121928 
2. Bonewald LF, Johnson ML. Osteocytes, mechanosensing and Wnt signaling. Bone. 2008;42(4):606-615. doi:10.1016/j.bone.2007.12.224 
3. Brotman RM, Shardell MD, Gajer P, et al. Association between the vaginal microbiota, menopause status, and signs of vulvovaginal atrophy. Menopause. 2014;21(5):450-458. doi:10.1097/GME.0b013e3182a4690b 
4. Cauley JA, Barbour KE, Harrison SL, et al. Inflammatory markers and the risk of hip and vertebral fractures in older men: the Osteoporotic Fractures in Men Study. J Bone Miner Res. 2016;31(12):2129-2138. doi:10.1002/jbmr.2905 
5. Cosman F, de Beur SJ, LeBoff MS, et al. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi:10.1007/s00198-014-2794-2 
6. Couse JF, Korach KS. Estrogen receptor null mice: what have we learned and where will they lead us? Endocr Rev. 1999;20(3):358-417. doi:10.1210/edrv.20.3.0370 
7. Darling AL, Millward DJ, Torgerson DJ, Hewitt CE, Lanham-New SA. Dietary protein and bone health: a systematic review and meta-analysis. Am J Clin Nutr. 2009;90(6):1674-1692. doi:10.3945/ajcn.2009.27799 
8. Dumoulin C, Cacciari LP, Hay-Smith EJC. Pelvic floor muscle training versus no treatment, or inactive control treatments, for urinary incontinence in women. Cochrane Database Syst Rev. 2018;10(10):CD005654. doi:10.1002/14651858.CD005654.pub4 
9. Fuentes N, Silveyra P. Estrogen receptor signaling mechanisms. Adv Protein Chem Struct Biol. 2019;116:135-170. doi:10.1016/bs.apcsb.2019.01.001 
10. Gandhi J, Chen A, Dagur G, et al. Genitourinary syndrome of menopause: an overview of clinical manifestations, pathophysiology, etiology, evaluation, and management. Am J Obstet Gynecol. 2016;215(6):704-711. doi:10.1016/j.ajog.2016.07.045 
11. Gillespie LD, Robertson MC, Gillespie WJ, et al. Interventions for preventing falls in older people living in the community. Cochrane Database Syst Rev. 2012;(9):CD007146. doi:10.1002/14651858.CD007146.pub3 
12. Guadalupe-Grau A, Fuentes T, Guerra B, Calbet JAL. Exercise and bone mass in adults. Sports Med. 2009;39(6):439-468. doi:10.2165/00007256-200939060-00002 
13. Harlow SD, Gass M, Hall JE, et al. Executive summary of the Stages of Reproductive Aging Workshop +10: addressing the unfinished agenda of staging reproductive aging. Menopause. 2012;19(4):387-395. doi:10.1097/gme.0b013e31824d8f40 
14. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-281. doi:10.1056/NEJMra070553 
15. Johansson H, Kanis JA, Odén A, et al. A meta-analysis of the association of fracture risk and body mass index in women. J Bone Miner Res. 2014;29(1):223-233. doi:10.1002/jbmr.2017 
16. Khosla S, Oursler MJ, Monroe DG. Estrogen and the skeleton. Trends Endocrinol Metab. 2012;23(11):576-581. doi:10.1016/j.tem.2012.03.008 
17. Manolagas SC. Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocr Rev. 2000;21(2):115-137. doi:10.1210/edrv.21.2.0395 
18. Maurel DB, Boisseau N, Benhamou CL, Jaffre C. Alcohol and bone: review of dose effects and mechanisms. Osteoporos Int. 2012;23(1):1-16. doi:10.1007/s00198-011-1787-7 
19. Mirmonsef P, Hotton AL, Gilbert D, et al. Free glycogen in vaginal fluids is associated with Lactobacillus colonization and low vaginal pH. PLoS One. 2014;9(7):e102467. doi:10.1371/journal.pone.0102467 
20. Morin M, Carroll MS, Bergeron S. Systematic review of the effectiveness of physical therapy modalities in women with provoked vestibulodynia. Sex Med Rev. 2017;5(3):295-322. doi:10.1016/j.sxmr.2017.02.003 
21. National Institutes of Health Office of Dietary Supplements. Calcium: fact sheet for health professionals. National Institutes of Health. Updated March 26, 2024. Accessed May 30, 2026. https://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/ 
22. Napoli N, Chandran M, Pierroz DD, Abrahamsen B, Schwartz AV, Ferrari SL; IOF Bone and Diabetes Working Group. Mechanisms of diabetes mellitus-induced bone fragility. Nat Rev Endocrinol. 2017;13(4):208-219. doi:10.1038/nrendo.2016.153 
23. North American Menopause Society, The. The 2020 genitourinary syndrome of menopause position statement of The North American Menopause Society. Menopause. 2020;27(9):976-992. doi:10.1097/GME.0000000000001609(NAMS) 
24. Peacock M. Calcium metabolism in health and disease. Clin J Am Soc Nephrol. 2010;5 Suppl 1:S23-S30. doi:10.2215/CJN.05910809 
25. Portman DJ, Gass MLS; Vulvovaginal Atrophy Terminology Consensus Conference Panel. Genitourinary syndrome of menopause: new terminology for vulvovaginal atrophy from the International Society for the Study of Women’s Sexual Health and The North American Menopause Society. Menopause. 2014;21(10):1063-1068. doi:10.1097/GME.0000000000000329 
26. Rahn DD, Carberry C, Sanses TVD, et al. Vaginal estrogen for genitourinary syndrome of menopause: a systematic review. Obstet Gynecol. 2014;124(6):1147-1156. doi:10.1097/AOG.0000000000000526 
27. Raz R, Stamm WE. A controlled trial of intravaginal estriol in postmenopausal women with recurrent urinary tract infections. N Engl J Med. 1993;329(11):753-756. doi:10.1056/NEJM199309093291102 
28. Reid IR, Bolland MJ. Calcium and/or vitamin D supplementation for the prevention of fragility fractures: who needs it? Nutrients. 2020;12(4):1011. doi:10.3390/nu12041011 
29. Riggs BL, Khosla S, Melton LJ III. Sex steroids and the construction and conservation of the adult skeleton. Endocr Rev. 2002;23(3):279-302. doi:10.1210/edrv.23.3.0465 
30. Rizzoli R, Stevenson JC, Bauer JM, et al. The role of dietary protein and vitamin D in maintaining musculoskeletal health in postmenopausal women: a consensus statement. Maturitas. 2014;79(1):122-132. doi:10.1016/j.maturitas.2014.07.005 
31. Seeman E, Delmas PD. Bone quality—the material and structural basis of bone strength and fragility. N Engl J Med. 2006;354(21):2250-2261. doi:10.1056/NEJMra053077 
32. Sözen T, Özışık L, Başaran NÇ. An overview and management of osteoporosis. Eur J Rheumatol. 2017;4(1):46-56. doi:10.5152/eurjrheum.2016.048 
33. Suckling J, Lethaby A, Kennedy R. Local oestrogen for vaginal atrophy in postmenopausal women. Cochrane Database Syst Rev. 2006;(4):CD001500. doi:10.1002/14651858.CD001500.pub2 
34. Tang BMP, Eslick GD, Nowson C, Smith C, Bensoussan A. Use of calcium or calcium in combination with vitamin D supplementation to prevent fractures and bone loss in people aged 50 years and older: a meta-analysis. Lancet. 2007;370(9588):657-666. doi:10.1016/S0140-6736(07)61342-7 
35. Turcotte AF, O’Connor S, Morin SN, et al. Association between obesity and risk of fracture, bone mineral density and bone quality in adults: a systematic review and meta-analysis. PLoS One. 2021;16(6):e0252487. doi:10.1371/journal.pone.0252487 
36. Ward KD, Klesges RC. A meta-analysis of the effects of cigarette smoking on bone mineral density. Calcif Tissue Int. 2001;68(5):259-270. doi:10.1007/BF02390832 
37. Weaver CM, Gordon CM, Janz KF, et al. The National Osteoporosis Foundation’s position statement on peak bone mass development and lifestyle factors: a systematic review and implementation recommendations. Osteoporos Int. 2016;27(4):1281-1386. doi:10.1007/s00198-015-3440-3 

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