Osteoporosis: A Female Targeted Condition

What is Osteoporosis?

Every year, millions of women experience fractures caused by osteoporosis, often without realizing their bones were weakening for decades. Osteoporosis is a bone disease characterized by reduced bone density and increased fragility. When osteoporotic bones experience even minor stress, a fragility fracture can occur. These fractures are most commonly found in the hip, spine, wrist, and forearm. Osteoporosis develops with age as the body's process of maintaining bone structure becomes unbalanced and old bone is broken down faster than new bone is formed (1).

In 2010, 10.3 million Americans over age 50 were diagnosed with osteoporosis, and a startling 80% of those individuals were women (3). 

Before we jump into the details of this condition, let's dive deeper into the bones themselves. A bone is made up of two different types of tissue: trabecular and cortical. Trabecular bone is a very lightweight, porous, and metabolically active tissue inside your bones. Its main function is to absorb shock and support joints (4). Cortical tissue is almost the exact opposite; it is the hard outer layer of your bone. Its compact nature helps provide strength and support for the body (5). 

Artwork by Shea Davis

Just as there are two types of bones, there are two types of osteoporosis. Type 1 osteoporosis is characterized by a significant loss of trabecular bone. Areas with a high percentage of trabecular tissue, like the spine, are likely to be severely affected. This form of osteoporosis predominantly affects women, particularly those who have gone through menopause in the last 10-15 years. Type 2 osteoporosis occurs when there is both cortical and trabecular bone loss, with more severe thinning of the former. This variant of the condition affects men and women more equally and typically appears around age 70 or later (1). 

The Biology of Osteoporosis

There are two main types of cells in the body that are responsible for bone function: osteoblasts and osteoclasts. When these cells stop working in balance, bone density begins to decline, and osteoporosis may develop (2). Our bodies are constantly undergoing a process called bone remodeling in order to replace old bone with new, healthier bone. Bone is removed by the osteoclasts in a process known as bone resorption, while bone is added by osteoblasts during bone formation (1). Normally, these two types of cells work together and are closely monitored by the body to ensure your bones stay healthy and dense. However, as we age, our bodies lose the ability to properly regulate bone remodeling, causing osteoclast activity to increase while osteoblast activity decreases (2). This means more bone is resorbed than formed, causing the bones to become weak.

The severity of low bone mass density is dependent not only on how quickly the bone is resorbed, but also on an individual's peak bone mass. From childhood through adolescence, there is fast bone formation as the body grows and strengthens. Bone formation continues more slowly after this period until maximum bone mass and strength are reached in a person’s 30s. From then on, bone density begins to decrease. Part of the reason osteoporosis is more prevalent in women is that females have a peak bone density around 10% lower than males (1). This means that when women start losing more bone than they form, they are more heavily impacted.

Osteoporosis and Estrogen

Sex hormones have many important roles in the body, including regulating bone remodeling. The two main classes of sex hormones are estrogens and androgens. While both hormones are present in both sexes, estrogen levels are higher in women, while androgen levels are higher in men. These differences in hormone levels are the primary reason osteoporosis affects men and women differently (2). Estrogens and androgens impact peak bone density, rate of bone mass decline, and the location of bone loss. The interaction between estrogen and osteoporosis has luckily been extensively studied, raising awareness about risks women face. 

We already know that women tend to have a lower bone mass than men. This is because estrogen helps regulate bone formation during puberty. Interestingly, females preferentially form cortical (remember this is the hard layer) bone from the inside of the bone because estrogen inhibits bone formation from the outside. Androgens have the opposite effect; they stimulate cortical bone growth on the outer surface. This leads to women having thinner bones than men. 

Next, recall that type 1 osteoporosis predominantly impacts newly postmenopausal women. During menopause, a woman's estrogen levels dramatically decrease. Estrogen plays an important role in regulating bone remodeling because it binds to osteoblasts to facilitate bone formation. When there is less estrogen, the osteoblasts simply don’t form bone as frequently. Additionally, less estrogen leads to higher rates of osteoclast formation, meaning more cells are now breaking down the bone (6). When we put this all together, it means decreases in estrogen lead to an unbalanced system where bone is broken down more than it is formed. Over time, this leads to low bone mass and eventually osteoporosis. 

In the first postmenopausal year, women lose approximately 5% of their bone mass with an additional 1-1.5% loss each subsequent year. By age 75, women are expected to have lost around 22% of their bone mass density, with the greatest impact seen in the spine and hips (1). Hip fractures present elevated concern as 60% of women are left unable to walk independently, 25% die within 1 year, and 25% must move to a nursing home (1). Osteoporosis is a severe and prevalent problem in elderly women and is expected to worsen if we don’t implement better prevention protocols (1).

Prevention, Testing, and Treatment

Doctors and researchers have developed a strong understanding of the biology of osteoporosis, especially in women. While this is fantastic progress, there are still issues with how the information is translated to clinical care. Unfortunately, most people are not diagnosed with osteoporosis until after a fracture has already occurred. The condition is largely asymptomatic until a bone fracture, but even when fragile fractures do occur, the condition remains underdiagnosed (1). Statistics from European women indicated 73% of those who need treatment for osteoporosis don’t receive it (1). Similarly, a survey in the U.S. found that only 31% of women reported receiving proper follow-up care following a fragile fracture, and 35% were unaware that osteoporosis was even the cause of their injury (1).

This data highlights the need for greater awareness, screening, and treatment to prevent fractures that could lead to detrimental health consequences. 

Osteoporosis and pre-requisite low bone density can be diagnosed using various X-ray imaging techniques (3,6). However, many individuals are currently diagnosed without such technology when they see a doctor for a fragile fracture (1). To move from treating fractures to preventing them, diagnosis needs to happen earlier in the patient’s life. The Bone Health and Osteoporosis Foundation recommends a scan examining bone mass density for all women 65 years and older every few years (1). Screening may be recommended as early as 50 if the individual exhibits risk factors for osteoporosis. Online surveys such as the Fracture Risk Assessment Tool can help individuals be aware of when they should seek screening.

Conclusion

Doctors and public health officials need to actively work towards early diagnosis and treatment to truly make a difference in women’s bone health. This includes educating patients about the condition and recommending early screening. Treatments for osteoporosis are highly effective at reducing fractures, but we need to get treatment to individuals before injury occurs to really make a difference in quality of life. We have the tools we need to reduce the consequences of osteoporosis, but we must use them effectively in clinical encounters to make meaningful change in elderly women's lives.

Citations

1. M. U. Keen, Osteoporosis in females. StatPearls [Internet]. (2025), (available at https://www.ncbi.nlm.nih.gov/books/NBK559156/).

2. Y.-Y. Zhang et al., Insights and implications of sexual dimorphism in osteoporosis. Bone Research. 12 (2024), doi:10.1038/s41413-023-00306-4.

3.  C. McPhee, I. O. Aninye, L. Horan, Recommendations for improving women’s bone health throughout the lifespan. Journal of women’s health (2002) (2022), (available at https://pmc.ncbi.nlm.nih.gov/articles/PMC9805882/). 

4. R. Oftadeh, M. Perez-Viloria, J. C. Villa-Camacho, A. Vaziri, A. Nazarian, Biomechanics and mechanobiology of Trabecular Bone: A Review. Journal of biomechanical engineering (2015), (available at https://pmc.ncbi.nlm.nih.gov/articles/PMC5101038/). 

5. C. J. Collins et al., in Encyclopedia of Biomedical Engineering (Elsevier, 2019; https://doi.org/10.1016/B978-0-12-801238-3.99937-9), pp. 22–44. 

6. S. Moghimikandelousi et al., Advances in biomonitoring technologies for Women’s Health. Nature News (2025), (available at https://www.nature.com/articles/s41467-025-63501-3).