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The Physiology behind Osteoporosis

Updated: Oct 21



Introduction


The human body undergoes numerous cycles throughout a lifetime, each marked by hormonal fluctuations. One significant phase is menopause, a natural occurrence in a woman's life around the age of 45-50, where the body undergoes a substantial hormonal shift. In this blog post, we will delve into the physiological changes that occur during menopause, specifically focusing on the impact of decreased estrogen levels on bone health (5).


Estrogen's Crucial Role


Estrogen, a group of hormones responsible for developing secondary female sex characteristics and regulating the reproductive system, plays a pivotal role in maintaining bone strength. Estradiol, the predominant estrogen before menopause, binds to estrogen receptors in the bones, initiating a cycle of bone building and breakdown. This intricate process involves communication between bone-building cells (osteoblasts) and bone-resorbing cells (osteoclasts), ensuring a delicate balance (5).


Menopause and Osteoporosis Risk

As menopause sets in, estrogen levels plummet, leading to a rapid decrease in bone density. This decrease is due to a disruption in the bone remodeling cycle, where the balance between osteoblasts and osteoclasts is compromised. The result is a net loss of bone tissue, making bones more fragile and prone to fractures (5).




Understanding Bone Remodelling


Bone remodeling is a continuous process involving four main types of cells – osteoblasts, extracellular matrix, osteoclasts, and osteocytes. Osteoblasts build up bone by synthesising the extracellular matrix, which is mineralised to form the bone structure. Osteoclasts, on the other hand, dissolve minerals and digest the bone matrix, allowing for remodeling. Osteocytes, derived from osteoblasts, act as the orchestrators, ensuring a harmonious balance between bone formation and resorption(1,4).


Bone remodelling, an ongoing process, involves four primary cell types with distinct functions:

  • Osteoblasts: Synthesize the extracellular matrix, a combination of various proteins crucial for bone strength.

  • Extracellular Matrix: Initially deposited as osteoid, it undergoes mineralization, transforming calcium into hydroxyapatite, a vital mineral in bones.

  • Osteoclasts: Dissolve minerals and digest bone matrix, facilitating bone resorption.

  • Osteocytes: Deriving from osteoblasts, these cells orchestrate the functions of both osteoblasts and osteoclasts, ensuring a harmonious bone remodeling process.


Bone Density

The bone density undergoes a dynamic process throughout life. In the first 25-30 years, density is built up, followed by a maintenance phase until around 40. After 40, a gradual decline begins, culminating in a rapid decrease during menopause. Over the 30-50 years of menopausal span, approximately 50% of trabecular bone and 30% of cortical bone are lost. The diagnosis of osteoporosis is made when bone density scores fall below <-2.5 standard deviation.



Conclusion

Understanding the intricate connection between hormonal changes, particularly the drop in estrogen levels during menopause, and the resulting impact on bone health is crucial. By shedding light on this often overlooked aspect of women's health, we hope to contribute to a broader conversation about proactive measures and awareness in addressing the challenges associated with osteoporosis during menopause.



Sources

  1. Anam, A.K. and Insogna, K. (2021) ‘Update on osteoporosis screening and Management’, Medical Clinics of North America, 105(6), pp. 1117–1134. doi:10.1016/j.mcna.2021.05.016.

  2. Aspray, T. and Hill, T. (2019) ‘Osteoporosis and the ageing skeleton’, Subcellular Biochemistry, pp. 453–476. doi:10.1007/978-981-13-3681-2_16.

  3. Hartley, G.W. et al. (2022) ‘Physical therapist management of patients with suspected or confirmed osteoporosis: A clinical practice guideline from the Academy of Geriatric Physical Therapy’, Journal of Geriatric Physical Therapy, 44(2). doi:10.1519/jpt.0000000000000346.

  4. LeBoff, M.S. et al. (2022) ‘The Clinician’s Guide to Prevention and treatment of osteoporosis’, Osteoporosis International, 33(10), pp. 2049–2102. doi:10.1007/s00198-021-05900-y.

  5. Mohamad, N.-V., Ima-Nirwana, S. and Chin, K.-Y. (2020) ‘Are oxidative stress and inflammation mediators of bone loss due to estrogen deficiency? A review of current evidence’, Endocrine, Metabolic &amp; Immune Disorders - Drug Targets, 20(9), pp. 1478–1487. doi:10.2174/1871530320666200604160614.

  6. Papadopoulou, S. K., Papadimitriou, K., Voulgaridou, G., Georgaki, E., Tsotidou, E., Zantidou, O., & Papandreou, D. (2021). Exercise and nutrition impact on osteoporosis and sarcopenia—the incidence of osteosarcopenia: A narrative review. Nutrients, 13(12), 4499. https://doi.org/10.3390/nu13124499

  7. Yang, T.-L. et al. (2019) ‘A road map for understanding molecular and genetic determinants of osteoporosis’, Nature Reviews Endocrinology, 16(2), pp. 91–103. doi:10.1038/s41574-019-0282-7.



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