PREGNANCY ASSOCIATED OSTEOPOROSIS

 “Motherhood is the biggest gamble in the world. It is the glorious life force. It’s huge and scary—it’s an act of infinite optimism.” — Gilda Radner
 

Pregnancy defines a challenging period to the mother's bones because the building of the fetal skeleton requires a substantial transfer of calcium. This process is particularly intense during the third trimester, when fetal bones experience substantial growth and calcification. The drainage of calcium from the mother has to bear some level of deterioration of the maternal skeleton unless compensatory mechanisms of enough potency are at play. If an adequate balance is not achieved, pregnancy would define a vulnerability period for maternal bones. Osteoporosis or even fragility fractures might be conceived whether the decalcifying process is particularly intense or whether there is an osteopenic background.





Bone metabolism during pregnancy

 

The main objective of calcium adjustments during pregnancy is to enable the adequate transplacental transfer of 30 g of calcium required for the successful mineralization of the fetal skeleton. Eighty percent of that amount is transferred during the third trimester.The fetus enjoys a status of persistent hypercalcemia, where a calcium placental pump maintains a gradient irrespective of the calcium status in the mother. This means that insufficiencies in the adjusting machinery in the mother will entail decalcification at her skeleton, something that may be a universal phenomenon at the third trimester, when the transfer of calcium increases drastically.


 



Main changes in the mother and the feto-placental unit that favor adequate transfer of calcium to the fetal skeleton. The calcium transferred to the fetus is provided by the mother. Three main domains, mother, placenta, and fetus.

The changes in the maternal domain include an increased intestinal absorption of calcium, where the role of vitamin D is still obscure. Further calcium supply is favored by maternal parathyroid hormone related-peptide (PTHrp) and by local changes within maternal bone, where receptor activator of nuclear factor kappa B ligand/osteoprotegerin (RANKL/OPG) and osteocytes may participate. The calcium drainage is partly counterbalanced by an increased anabolic process, where IGF1, stimulated by placental growth hormone (PGH), may be involved. Other potential agents are prolactin (PRL) and estrogens (E). Despite the reactive bone formation process, the bone balance seems negative for the mother. The placental calcium gradient is sustained by the placental pump, where fetal PTH and PTHrp are determinant.


The status of the skeleton in pregnancy


The deterioration of bone density accelerates during lactation, when maternal bone is the main source of the considerable amounts of calcium provided with breast milk. However, the rapid loss in bone mineral density (BMD) during lactation, which may attain 5–10% in 2–6 months, restores along the 6–12 months after weaning through still unclear mechanisms. This fast recovery is reflected in epidemiological studies, which do not find an association between the number of pregnancies or the duration of lactation and the future diagnoses of either osteoporosis or fragility fracture.

 




Osteoporosis during pregnancy


The transitory deterioration of maternal bone during pregnancy leads to increased bone fragility. Osteoporosis may indeed occur if concomitant conditions, such as baseline osteopenia, or other predisposing circumstances, are present. Prevalence is unknown because the main diagnostic methods involve radiation, which is usually avoided in pregnant women.

 

The main clinical symptom is severe and persistent back pain, which usually occurs at the end of pregnancy or early puerperium. The high prevalence of back pain in women during advanced pregnancy explains the poor attention received, and the consequent low number of diagnoses. When suspected, imaging techniques should help in clarifying the diagnosis. Cortical bone may be affected as well. The hip is then the preferred territory, as it occurs in the form of the disease so prevalent in older women. Hip fracture may then present as an additional complication.







Pregnancy associated osteoporosis (also called transient osteoporosis of pregnancy) is a rare condition where a woman’s bones break easily during pregnancy or in the weeks after she has given birth. These breaks normally occur in the spine, and sometimes the hip. While this can be painful and debilitating for a time, the bones usually heal quickly and most women recover fully without their daily lives being affected. Pregnancy associated osteoporosis is generally short-lived, and most women who have had this condition do not suffer broken bones in later pregnancies.




CAUSES

It is possible that some women already have low bone density before they become pregnant, as a result of chronic disease, medications or lifestyle, and the increases in bone metabolism that occur naturally in pregnancy bring added stresses to the skeleton.

 Pregnancy also places more demands on the skeleton’s ‘calcium bank’. A healthy diet with adequate calcium and vitamin D levels will normally meet this demand, but in a small proportion of women, inadequate calcium and vitamin D may lead to excessive ‘withdrawals’ from the bank and a weakening of the bones during pregnancy.

 Some women need to have heparin injections during their pregnancy to treat a serious condition called anti-phospholipid syndrome. Heparin has been associated with pregnancy associated osteoporosis in some but not all research studies .

Large decreases in bone mineral density (BMD) may increase susceptibility to osteoporotic fractures. All women lose BMD during pregnancy and breastfeeding, but this is usually regained naturally after weaning and does not cause issues.

Women with PAO may:

 • Experience a greater drop in bone mineral density relative to the average and/or

 • Enter pregnancy with a low baseline BMD, making them more susceptible.

 

RISK FACTORS

PAO can occur with no apparent risk factors (idiopathic . Some risk factors have been identified in some women who develop PAO:

• Inadequate nutritional intake before or during pregnancy impacting bone health:

• Hyperemesis

 • Coeliac Disease, Crohn’s or other malabsorption issue.

• Dietary restrictions (i.e. vegan diet without adequate calcium intake, and nutrients vital to health and wellbeing)

• History of eating disorder or low BMI (<20)

·  PAO diagnosed in a previous pregnancy

• Osteopenia or osteoporosis diagnosed prior to pregnancy

• History of fractures prior to pregnancy, including childhood

• Family history of osteoporosis or fragility fractures

• Genetic variants leading to bone formation issues

• Amenorrhea, exercise-induced or otherwise

• Renal stones/hypercalciuria

 Medical treatments that may negatively impact BMD:

 • Progestogen-only contraception (including Depo-Provera)

• Anticoagulants before or during pregnancy (including low molecular weight heparin)

• Thyroid hormone

• Corticosteroids

 • History of cancer treatment






SIGNS AND SYMPTOMS


1. Pain Presentation

 • Persistent back or hip pain not fully explained by the birth or following caesarean section recovery.

• Sudden intense back and/or hip pain (“sensation of an electric pop”) with low impact (e.g. putting baby in cot) or equally no impact, occurring in late pregnancy, during labour or in the first few months after giving birth.

• Severe back or hip pain, with or without difficulty walking, affecting, everyday functioning. This can be misdiagnosed as pelvic girdle pain in pregnancy or postnatal depression in the first trimester.


2. Sensation of pain or pain symptoms

• Reported feeling unable to hold up their own bodyweight due to pain

• Described as crushing or squeezing pain in the chest or back

• Pain radiating from back to the ribcage

• Loss of arm strength or inability to raise arms above shoulder-height without severe pain 

• Painful muscle spasms, particularly in the back

• Cracking/popping sounds in spine during certain movements, accompanied by severe pain

 • Collapsing with pain

 

3. Reduced functioning due to pain

• Significantly affecting daily function (i.e. difficulty with dressing, bathing, walking, moving from sitting to standing position, sleeping, moving in bed, travelling in a car, caring for baby)

• Reduced mobility (i.e. use of walking aids when not usually required, housebound etc)

• Difficulty weight bearing on hips

• Difficulty with breastfeeding (i.e. unable to: feed sitting up, support weight of baby in arms)

• Progression of pain

• Pain improves for a short period before getting significantly worse, possibly due to further fractures occurring, with a further reduction in functioning

• Pain improves as fractures heal but pain may be prolonged due to changes in biomechanics and joint loading as well as irritation of the nerves and muscles around the spine.

• Pain that is reported as electric, shooting, knife-like may indicate nerve pain

• Pain may resolve fully in time, although improvement with bone density is slow

 

4.  Physical appearance changes

• Loss of height

• Curved or Kyphotic posture (rounded back) 


TREATMENT

There is no standard protocol to date. In addition to rest, movement modification, treatments to ease pain and nutritional support, appropriate specialist may be required and could include:

• GP, coordination of specialists, assessment of nutrient deficiencies through blood tests, elimination of other causes of low BMD and fracture (e.g. Myeloma/bone cancer)

Rheumatologist: medical management of osteoporosis, including medications

Endocrinologist: medical management of osteoporosis and/or hormonal conditions impacting bone health

Neurosurgeon: assessment of spinal fragility and guidance on rehabilitation. In selective cases, treatment may include vertebroplasty, although rarely used now.

Nutritionist: guidance regarding dietary chances to support bone health

Osteoporosis physiotherapists: enable safe return to movement and strength-building. In the UK, doctors with specialist experience in PAO will assess and determine whether to let women’s bones heal naturally or to prescribe osteoporosis medicines like bisphosphonates or teriparatide based on several factors including their bone density and whether they keep fracturing.


PROGNOSIS

The trajectory of this rare condition is not fully understood. Some women make full recoveries, either naturally or with medical assistance, whilst others may require ongoing treatment of osteoporosis and/or secondary impact of fractures (i.e. chronic pain) for a prolonged period (years or decades). Some women will experience fractures in subsequent pregnancies.

 

Supporting an early diagnosis of PAO:

• Healthcare professionals need to take self-reports of debilitating pain seriously as women with PAO have reported that their pain was dismissed or misdiagnosed.

• Refer for x-ray or MRI if pain and struggling to care for their baby has a significant impact on a woman’s daily living activities.

• Physiotherapists, osteopaths and chiropractors should consider referring pregnant or postpartum women further assessment (i.e MRI/xray) before treating them, if they present with symptoms indicating possible PAO fractures.

• Once fractures are identified urgent referral to the osteoporosis service should be made.

• Medical tests should rule out other underlying fracture causes, so the appropriate treatment can be given.

• PAO should be ruled out, if low or no impact fractures occur during pregnancy or postpartum.


 Ideally, support with management of the disease should include:

• Urgent referral to local osteoporosis service, physiotherapy and pain management

 • Consultation with National PAO expert services to determine best practice.

• Osteoporosis medications are not compatible with breastfeeding, so will need to be delayed until cessation of breastfeeding.

• Assess mental health and refer to specialist services, as PAO can significantly impact on mental wellbeing.

• Refer to occupational therapy for advice on daily activities and baby care as indicated

 


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