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Aging and bone health
Peak bone mass achieved at about age 25 years is largely determined by genetic factors, although extreme malnutrition, impaired reproductive status, paralysis, and severe chronic illness may cause a significantly lower peak bone mass. Bone is an active organ with a normal physiology of removing older bone and replacing with new matrix to achieve tensile strength through a three-dimensional architecture of cross-linked and calcified proteins.
Aging is associated with reductions in the synthesis of new bone matrix proteins, while menopausal reductions in sex and adrenal hormones for women result in accelerated resorption of existing bone. Age-related male endocrine changes have less clinical impact as men have greater peak bone mass than woman and sex steroid decreases occur more gradually than menopausal endocrine changes. Reductions in sun exposure and inadequate vitamin D intake place some older adults at risk for impaired bone mineralization.
Osteoporosis is the common disorder of compromised bone architecture and reduced tensile strength that contributes greatly to fractures with aging, estimated to occur in half of Caucasian women and one in five men.[1] Although osteoporosis is less common in African Americans, those with osteoporosis have the same fracture risks as Caucasians. Fractures result when weakened bone is overloaded, often by falls or lifting heavy objects.
Hip fractures are a significant consequence of osteoporosis and are associated with excess mortality, ranging from 8% to 36% at one year, with higher mortality in men than in women. Vertebral and pelvic fractures contribute to gait disorders and can cause disabling back or pelvic pain. Severe kyphosis resulting from vertebral fractures in addition to age-related degenerative changes of the spine may contribute to restrictive lung disease, impaired bowel function, and limited mobility.
Osteoporosis screening
The US Preventive Services Task Force (USPSTF) recommends bone mineral density testing for women >65 years of age, and for younger adult women who have fracture risks comparable to those of an otherwise healthy 65-year-old woman,[2] estimated by the World Health Organization (WHO) Fracture Assessment Tool as a 10-year risk of about 9.3% (forearm, shoulder, clinical spine, and hip fracture). However, the Women’s Health Initiative Study reported in 2014 that a Simple Calculated Osteoporosis Risk Estimate (SCORE) >7 or an Osteoporosis Self-Assessment Tool calculated as 0.2 × (weight in kg – age in years) < 2 were more predictive of low bone density for postmenopausal women aged 50–64 than the Fracture Risk Assessment >9.3%.[3]
The National Osteoporosis Foundation recommends bone mineral density testing in men >70 years of age,[4] although the USPSTF cites insufficient data to recommend screening bone density in men.[2] All agree that postmenopausal women and men over age 50 who experience a low-impact adult fracture of the hip, spine, pelvis, humerus, or forearm should undergo bone mineral density testing and consideration for osteoporosis drug therapies.
Medical conditions and certain drug therapies are associated with bone loss (Table 32.1). Fall risk is a consideration when determining need for bone mineral density testing. Fall risks are associated with neurologic conditions that impair gait and balance, cardiac conditions that predispose to orthostasis, and musculoskeletal conditions that impair gait such as degenerative and inflammatory arthritis and degenerative spine.
| Endocrine | Gastrointestinal | Hematologic | Neurologic | Other |
|---|---|---|---|---|
| Diabetes mellitus | Celiac disease | Monoclonal gammopathy | Stroke | Familial hypercalciuria |
| Central obesity | Inflammatory bowel diseases | Systemic mastocytosis | Parkinson’s disease | Chronic kidney disease |
| Hyperparathyroidism | Short gut syndrome | Chemotherapy | Antiseizure medications | Rheumatoid arthritis |
| Thyrotoxicosis | Bariatric surgery | Radiation therapy | Systemic steroid therapy | |
| Cushing syndrome | Chronic anti-acid therapy |
Dual energy x-ray absorptiometry is considered the most cost-effective bone mineral density technique,[5] although for older adults, degenerative changes of the spine may give falsely elevated results. The proximal radius and hip are two additional sites for clinical measurement. The WHO defines osteoporosis using only the mean lumbar spine (at least two vertebral bodies), total hip, proximal femur, and proximal radius bone sites. Osteoporosis is defined by bone density criteria as bone mineral density of at least one of these bone sites more than 2.5 standard deviations below normal gender peak specific bone mass (T score ≤–2.5). Normal bone density is defined by the WHO as a bone density greater than one standard deviation below normal peak bone mass, (T score ≥–1.0), with osteopenia T score between –1 and –2.5.
Alhough other technologies exist to measure bone density, dual energy x-ray absorptiometry is preferred based on access, radiation exposure, and cost. Quantitative CT scanning has greater radiation exposure and cost; ultrasound techniques, while portable and low cost, limit the bone sites for measurement and cannot be used for serial monitoring of osteoporosis treatments.
The clinical history and physical exam determine the need for additional diagnostic studies beyond bone densitometry. For example, a bone density that is significantly below that expected for age and gender in the setting of comorbid conditions of migraine syndrome and GI symptoms of bloating may prompt studies for celiac disease. Evaluation of hypercalcemia or renal calculi associated with osteoporosis includes serum intact parathyroid hormone and 24-hour urine collection to assess for hypercalciuria.
Without additional clinical findings of comorbid medical conditions, further diagnostic studies before offering drug therapies for postmenopausal or age-related osteoporosis include assessment of renal function, serum calcium, and serum 25-hydroxyvitamin D3.
Osteoporosis treatments
Bone health nutrition
A heart healthy diet may not meet the nutritional needs for bone health because fresh fruits, vegetables, and lean meats contain small amounts of calcium and vitamin D. The addition of low- and no-fat dairy products, plant milk (such as soy and almond milk), calcium-fortified beverages (such as calcium-fortified fruit juices), and foods such as breakfast cereals can achieve a bone healthy diet without compromising cardiovascular health. Optimal calcium intake is 1,000 mg elemental calcium daily through dietary sources, although older adults taking loop diuretics may require 1,200 mg to account for calcium loss resulting from diuresis. In contrast, thiazide diuretics conserve calcium from renal loss.
For those who cannot obtain adequate calcium intake through diet alone, calcium supplements are available in various formulations – tablets, soft chews, gummies, and dissolvable powders – but may cause gas, bloating, and constipation to a greater extent than dietary sources. Anti-acid drugs, such as H2 blockers and proton pump inhibitors, impair digestion of calcium, although calcium citrate supplements do not require gastric acid for digestion. Clinical trials have demonstrated an association among calcium supplementation and increased risk of cardiovascular disease;[6] however, a systematic review considering benefits/risks of adequate calcium and vitamin D intake in treating osteoporosis concluded that adequate, but not excessive, supplementation of bone nutrients is appropriate osteoporosis management for those with comorbid cardiovascular conditions.[7]
Vitamin D deficiency in the elderly can result in deep bone and muscle pain, muscle weakness, hyperesthesia, as well as fractures from brittle bone that lacks calcium deposition, called osteomalacia. Vitamin D is the hormone that facilitates calcium absorption from the gut. Changes in skin metabolism and decreased sun exposure are thought to contribute to vitamin D deficiency in older adults. Daily intake of 800 units of vitamin D is adequate to prevent vitamin D deficiency for most older adults, with higher dose supplements needed for those with GI malabsorption, including those with acquired celiac disease (allergy to gluten, a protein found in wheat and other related grains).[8]
Drug therapies for osteoporosis
FDA approved drug therapies are antiresorptive agents that prevent further bone loss, with the exception of teriparitide, an anabolic therapy that stimulates new bone protein formation, though to a lesser degree also stimulates osteoclastic bone resorption. The American Academy of Clinical Endocrinologist guidelines on osteoporosis drug therapies include first-line agents alendronate, risedronate, zoledronic acid, and denosumab because all have been shown in clinical trials to reduce vertebral, nonvertebral, and hip fractures (Table 32.2).[9] Alendronate and risedronate are preferred over zoledronic acid and denosumab due to lower cost and oral administration.
| Fracture risk reduction | |||||
|---|---|---|---|---|---|
| Drug | Class | Route of administration | Vertebral | Nonvertebral | Hip |
| Alendronate | Bisphosphonate | Oral weekly | Yes | Yes | Yes |
| Risedronate | Bisphosphonate | Oral weekly or monthly | Yes | Yes | Yes |
| Zoledronic acid | Bisphosphonate | Intravenous once yearly | Yes | Yes | Yes |
| Denosumab | Monoclonal antibody against RANK-L receptor | Subcutaneous every 6 months | Yes | Yes | Yes |
| Ibandronate | Bisphosphonate | Oral monthly or intravenous every 3 months | Yes | * No effect demonstrated | * No effect demonstrated |
| Raloxifene | Selective estrogen receptor modulator | Oral daily | Yes | * No effect demonstrated | * No effect demonstrated |
| Teriparatide | Synthetic parathyroid hormone derivative | Subcutaneous daily | Yes | Yes | * No effect demonstrated |
| Calcitonin | Synthetic salmon calcitonin | Intranasal daily or subcutaneous daily | Yes | No effect demonstrated | No effect demonstrated |
* The lack of demonstrable effect at these sites may be due to insufficient sample size for study.
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