Bone health and pregnancy: Osteoporosis and beyond

The physiological demands of pregnancy and lactation necessitate substantial adaptations in maternal mineral metabolism, with significant effects on skeletal integrity [1,2]. While osteoporosis of the hip remains the most commonly discussed bone complication of pregnancy, this limited focus fails to capture the broader implications of pregnancy-induced bone remodelling. Gestation and lactation represent periods of accelerated and dynamic skeletal turnover, characterized by increased calcium mobilization, alterations in hormonal regulation (e.g., parathyroid hormone-related protein, oestrogen, calcitonin), and shifts in bone resorption and formation [3,4]. These processes may have long-term consequences for maternal bone health, especially in women with preexisting metabolic risk factors. Therefore, effective management of metabolic health and bone disorders during pregnancy and lactation requires a nuanced approach to meet the dual needs of the mother and fetus (Fig. 1) [5].

Fig. 1.

The relationship between hormonal and metabolic adaptations in pregnancy, bone and joint diseases such as osteoporosis in women, highlighting health inequities and research gaps.

Bone serves as a critical mineral reservoir that undergoes coordinated remodelling during pregnancy to support maternal–foetal mineral homeostasis [1,4]. Pregnancy represents an important period of physiological adaptation in mineral metabolism to meet the demands of the developing fetus [1]. The physiological requirement for calcium increases substantially in pregnancy, especially in the third trimester, driven by foetal skeletal mineralization [1]. In response, maternal physiology enhances calcium absorption in the intestine, primarily via upregulation of 1,25-dihydroxyvitamin D (calcitriol), leading to a two- to three-fold increase in intestinal calcium absorption [6]. Renal handling of calcium also adapts, although hormonal regulation is central to this adaptation. Parathyroid hormone-related peptide (PTHrP), produced by the placenta and breasts, rises significantly during pregnancy and lactation, contributing to maternal bone resorption and calcium mobilization. Oestrogen levels increase and exert a protective effect on the skeleton by inhibiting bone resorption, while endogenous calcitonin production may help buffer against excessive bone loss [7].

Despite these mechanisms, most clinical studies have shown increased bone turnover during pregnancy, with elevated biochemical markers of bone resorption [8] and, to a lesser extent, bone formation. These changes reflect the bone's active role in maternal adaptation, providing calcium through controlled and reversible skeletal remodelling. Understanding this dynamic interplay is essential for appreciating pregnancy as a unique window into bone physiology rather than solely a risk factor for osteoporosis [9].

While osteoporosis remains a central focus in maternal skeletal health, pregnancy can precipitate a range of musculoskeletal disorders that extend beyond bone fragility and fracture risk, and this has been discussed in a number of recent case reports [10,11]. Transient osteoporosis of pregnancy (TOP), often affecting the hip in the third trimester or early postpartum, presents with acute pain and functional limitation [12,13]. Though typically self-limiting, TOP can be difficult to diagnose and manage, particularly in settings with limited access to advanced imaging. Pregnancy- and lactation-associated osteoporosis (PLO) [10] is a rarer but clinically significant entity, characterized by fragility fractures, most commonly vertebral, that occur in late pregnancy or during lactation. The predisposing susceptibilities to PLO include high BMI, prior family history, poor diet, use of corticosteroids (e.g. for asthma or autoimmune diseases), or use of antiepileptic agents which can affect bone metabolism. The pathophysiology likely reflects exaggerated physiological bone resorption to meet foetal and neonatal calcium demands, particularly in women with low baseline bone mass, inadequate calcium and vitamin D intake, or prolonged exclusive breastfeeding [14]. Bone mineral density often improves after weaning in PLO, but full reversibility, especially regarding fracture risk and bone microarchitecture, cannot be assumed. Therefore, a period for spontaneous recovery should be allowed before considering targeted pharmacologic treatment, if clinically indicated.

In addition to osteoporosis, clinicians should be vigilant for other skeletal complications including stress fractures, postpartum sacral insufficiency fractures [15,16], and bone marrow oedema syndromes. These conditions are underdiagnosed and may be misattributed to common musculoskeletal complaints of pregnancy. Joint laxity, driven by hormonal changes such as elevated relaxin, also contributes to musculoskeletal pain and increased risk of injury. Importantly, there is growing recognition that racial and ethnic disparities influence the prevalence, diagnosis, and outcomes of these bone disorders, although data specific to under-recognized conditions remain scarce and warrant further investigation [17]. Women from under-represented or marginalized backgrounds may experience differential access to care, lower rates of diagnosis, and variations in bone metabolism due to genetic and sociocultural factors [4,18]. Future research and clinical practice must therefore actively account for these disparities to improve equity in maternal bone health.

Pain during pregnancy, particularly musculoskeletal pain, is another common but often under-recognized component of maternal bone health and is difficult to treat [19]. It is also important to highlight under-recognized bone conditions that may either be pre-existing and worsen or present for the first time during pregnancy and lactation. These include rare but serious disorders such as Paget's disease, osteogenesis imperfecta, rickets and osteomalacia (nutritional as well as congenital and other acquired forms), and avascular necrosis (AVN) [5,20,21]. While data on these conditions in the context of pregnancy are limited, their occurrence may complicate maternal and foetal outcomes and they are often missed due to overlapping symptoms with more common musculoskeletal complaints. Increased clinical awareness and targeted screening protocols could significantly improve early recognition and management of these disorders [22,23].

There is a lack of large-scale, longitudinal studies examining the long-term skeletal consequences of pregnancy and lactation [24]. Most published data are restricted to case reports or very small cohorts, restricting our understanding of recovery trajectories and risk of future osteoporotic events. Current clinical care pathways rarely include bone health screening in young or postpartum women, even among those with known risk factors such as pre-existing low bone mass, eating disorders, vitamin D deficiency, autoimmune diseases, short interval between pregnancies, or prolonged exclusive breastfeeding. This oversight represents a significant gap and a missed opportunity for early intervention and risk mitigation.

Maternal bone health encompasses a spectrum of physiological adaptations and clinical challenges beyond osteoporosis. Recognizing pregnancy and lactation as periods of skeletal vulnerability and opportunity demands increased clinical awareness, multidisciplinary collaboration, and targeted research [24]. This includes addressing racial, ethnic, and geographic disparities in risk, diagnosis, and access to care. Advancing maternal musculoskeletal health requires integrating obstetric, rheumatologic, and endocrinologic expertise to inform prevention, early detection, and culturally relevant public health strategies. Conditions such as sacroiliac joint dysfunction, bone marrow oedema syndromes, and pregnancy-associated fractures can cause significant morbidity. Understanding and addressing these conditions is essential for optimizing function and quality of life during and after pregnancy. Effective treatment must consider the implications for the mother and fetus, optimizing non-pharmacological therapeutic options [25]. Fortunately, with early detection, the lost bone mass associated with pregnancy and lactation can often be regained, though the extent of recovery varies and requires careful monitoring.