madman
Super Moderator
Osteoporosis
Review of Etiology, Mechanisms, and Approach to Management in the Aging Population (2023)
Sonali Khandelwal, MD,Nancy E. Lane, MD
Osteoporosis, the most common metabolic bone disease, is characterized by low bone mineral density (BMD) and reduced bone strength, and this results in an increased risk for fractures. It is a significant health problem, particularly affecting the aging population.
This article provides an update on the epidemiology, etiology, and approach to the diagnosis of osteoporosis in the aging population.
The prevalence of low bone mass and osteoporosis is high. An epidemiologic study determined that low femoral bone density is present in 14,646 US men and women from the Third National Health and Nutrition Examination Survey (NHANES III).1 According to the World Health Organization (WHO) criteria that use T scores (standard deviations below peak bone mass), this survey revealed that 13% to 18% of women aged 50 years or more had osteoporosis and another 37% to 50% had osteopenia. Applying these numbers to the most recent US census data in 2010 translates to over 10 million individuals with osteoporosis and over 20 million with osteopenia.1 Worldwide, approximately 200 million women have osteoporosis.2 Overall, the age-adjusted prevalence of osteoporosis among adults aged 50 and over has increased from 9.4% in 2007–2008 to 12.6% in 2017–2018. The prevalence of osteoporosis among women has increased from 14.0% in 2007–2008 to 19.6% in 2017–2018. However, osteoporosis prevalence in men did not significantly change from 2007–2008 (3.7%) to 2017–2018 (4.4%) (Fig. 1).
In the United States, 250,000 individuals aged 65 or greater fracture their hip each year.3–5 Hip fractures increase exponentially with age: the incidence of hip fractures in white women (per 1000 person-years) is 2.2, for ages 65 to 69 years; 4.4, for ages 70 to 74 years; 9.5, for ages 75–79 years; 16.9, age 80 to 84 years; 27.9, age 85 to 90 years; and 34.2, age 90 years and older.3,5 Hip fractures have long been considered one of the most devastating osteoporotic-related fractures due to postfracture disability and immobility. Unfortunately, hip fractures are projected to increase from an estimated 1.7 million in 1990 to 6.3 million by the year 2050.5,6 In addition, ethnic variations in bone mass have been noted in population studies.6 African Americans have higher and Asian Americans have lower BMD than White Americans.6 Moreover African Americans have lower fracture rates at many skeletal sites, including hip, clinical vertebral, upper, and lower appendages. In addition, Hispanic Americans and Asian Americans also have lower hip fracture rates than White Americans.6 In the United States for Caucasian ethnicity, it is currently estimated that the lifetime risk by age 50 of having a hip fracture is about 16% to 17.5% for women and 5% to 6% for men. For African Americans, the lifetime risk is lower but estimated to be 5.6% and 2.8% for women and men, respectively. Although the likelihood of developing osteoporosis is currently greatest in North America and Europe, as population longevity in developing countries increases so will the risk of osteoporosis.2
ETIOLOGY OF BONE LOSS IN AGING
Osteoporosis is a skeletal disorder characterized by compromised bone strength as well as bone quality predisposing to an increased risk of fractures. Normal bone remodeling involves an equilibrium between the process of bone resorption in which osteoclasts remove the bone by acidification and proteolytic digestion and bone formation in which osteoblasts secrete osteoid matrix into the resorption cavity.7 Activation of the remodeling cycle serves two functions in the adult skeleton (1) produce a supply of calcium to the extracellular space and (2) provide elasticity and strength to the skeleton. When the remodeling process is uncoupled there is either excess resorption of bone leading to bone loss versus excess bone acquisition when formation exceeds remodeling.8 In the bone remodeling process, osteoblasts are activated through various mechanisms including growth hormone, and parathyroid hormone (PTH). M-CSF and receptor activator of nuclear factor kappa-B ligand (RANKL) are the two major osteoblast-mediated factors, which regulate the recruitment of osteoclasts.7
In older individuals, there is an uncoupling of the bone remodeling cycle due to several factors, including a reduction in the number of activity of osteoblasts, so the amount of time to fill in resorption cavities is longer, and an increase in low-grade systemic inflammation, especially pro-inflammatory cytokines (TNF, IL-1, and IL-6) that seems to increase the number and activity of osteoclasts. Over time in older individuals, there is a net loss of bone. In addition to the uncoupling of bone remodeling with aging, the compromise of other major organs, such as the kidney reduces the activation of 25 D to 1.25 D which reduces the amount of calcium absorbed from the gastrointestinal tract, and a negative calcium balance ensues, and osteoclasts are required to resorb calcium to fill this gap.
In addition to uncoupling of normal bone homeostasis, inherent bone quality contributes to the risk of poor bone health. Small bone size, disrupted microarchitecture, cortical porosity, compromised quality of bone, and decreased viability of osteocytes are some biological factors contributing to decreased strength over time.8–10 A major determinant of bone density in an older individual is his or her peak bone mass.11,12 Peak bone mass is the maximum bone mass achieved in life. The time of peak bone mass is not known with certainty, but probably occurs in the third to fourth decade of life in most individuals, with differences in timing due to genetic, hormonal, and environmental variables and to the skeletal site (type of bone) and method of BMD measurement.11
In addition to the uncoupling of bone turnover, which is so common in aging, estrogen deficiency is also a critical factor for the development of osteoporosis in both women and men. Age-related bone loss may begin immediately after the acquisition of peak bone mass for either sex, however, most bone loss occurs after the age of menopause in women and after the age of 70 years in men.10 Nevertheless, it is unknown what contributes greater; to the molecular events causing disequilibrium between bone resorption and formation in aging versus sex steroid deficiencies.9 At menopause, there is a somewhat fast decline in ovarian function in women and a slower decline of both androgen and estrogen levels in men with advancing age, the two conditions inexorably overlap, making it impossible to separate their independent influence from the cumulative anatomic deficit.8 In Caucasian women aged 65 and older, both low serum total estradiol and high serum concentrations of sex hormone-binding globulin have been shown to increase the risk of hip and vertebral fractures without relation to BMD.10 Interestingly, mouse models of bone loss suggest that the adverse effects of old age on the skeleton are independent of estrogens and are due to molecular mechanisms that are distinct from those responsible for the effects of sex steroid deficiency.13–16
Suggested causes of bone-intrinsic molecular mechanisms include mitochondria dysfunction, oxidative stress, declining autophagy, DNA damage, osteoprogenitor, osteocyte senescence, senescence-associated secretory phenotype, and lipid peroxidation.14 Age-related changes in the bone resulting from intracellular reactive oxidative species (ROS) are not a new concept, but it has recently been proposed as a contributor to osteoporosis, especially in the older. ROS are generated during fatty acid oxidation and in response to inflammatory cytokines and it is suggested that both estrogens and androgens may protect against oxidative stress.15,16 In addition, estrogen withdrawal and deficiency at menopause are also believed to cause increased production of inflammatory cytokines and promote T-cell activation.17–19 The loss of estrogen results in the activation of specific T-cell subsets including T helper cells that support the production of IL-17, RANKL, IL-1, TNF, and IL-6 that stimulate osteoclast maturation, activity, and a lifespan that seem to prolong their lifespan and inhibit osteogenesis. In addition, estrogen deficiency and aging reduce the number and activity of Treg cells that reduce the production of inflammatory cytokines. These events that alter the immune system and inflammation with estrogen deficiency seem to increase with the addition of aging. Mouse models reveal the loss of estradiol due to ovariectomy increases osteoclast formation along with colony-forming units for granulocytes and macrophages in vitro. Similarly, this deficiency increases the number of osteoclasts in trabecular bone in animals. Along with elevated T cells, postmenopausal deficiency also stimulates B-lymphopoiesis. There has been a direct relationship observed between elevated B cells and bone resorption.
In addition to the normal aging process and menopause, there are many other clinical, medical, behavioral, and nutritional risk factors involved in the etiology of bone loss in the aging population.9 Clinical risk factors to consider include body mass. Older individuals with low body weight, low percentage of body fat, or low body mass index are at an increased risk of low bone mass and rapid bone loss.20 In addition, a history of prior fractures is extremely relevant as several studies have documented associations between prior fracture history at any site and risk of future vertebral and hip fractures and a first-degree relative having a history of a hip fracture.10,21–23 Moreover, in women who have developed an incident vertebral fracture, 1 in 5 develop a new incident vertebral fracture in the subsequent year.22 Impaired vision independently increases the risk of hip fracture in older white women10 and contributes to the risk for falls which is another independent risk factor for fracture. Finally, poor hand grip strength, a component of the definition of frailty, which can be caused by cognitive decline, diabetic neuropathy, or pain is a strong independent risk factor for fragility fractures in postmenopausal women.23
Several medical disorders as well as medications listed in Table 1 are associated with secondary osteoporosis in the aging population. This table albeit not fully inclusive of all conditions demonstrates the number of comorbidities that are highly prevalent in the older and can interfere with bone health. These disorders include gastrointestinal disorders (eg, inflammatory bowel disease, malabsorption syndromes, and celiac), hematologic disorders (eg, leukemia and lymphoma), endocrine disorders (eg, diabetes, hyperparathyroidism), and neurological disorders (eg, Parkinson’s disease, stroke), and renal insufficiency.24,25 In addition, exposure to certain medications may contribute to and/or increase the risk of bone loss. Glucocorticoids are the most implicated class of medication, affecting both bone quality and quantity of bone.26 Several studies investigating glucocorticoid-induced bone loss suggest that the degree of increased risk of vertebral fracture in glucocorticoid-treated men and women is disproportionate to observed decreases in BMD, leading investigators to surmise that in addition to reducing bone mass, glucocorticoid treatment may lead to bone quality defects mediated by increases in bone turnover and trabecular thinning.26,27 Other medications to consider are aromatase inhibitors, proton pump inhibitors, anticoagulants (heparin), selective serotonin reuptake inhibitors, and thiazolidinediones.
Behavioral factors have also been linked to the development of bone loss in older adults and include cigarette smoking, poor physical activity, and alcohol abuse. Cigarette smoking is believed to induce bone loss and increased hip fracture risk in the older part due to various mechanisms: (1) direct toxic effect on osteogenesis,28,29 (2) collagen metabolism in combination with increased bone resorption and osteoclast activity and osteoclastogenesis,30 (3) calciotropic hormone metabolism, (4) dysregulation of sex hormones,31 and (5) decreased intestinal calcium absorption.20,32,33 Some studies have suggested low levels of physical activity in the older, especially weight-bearing activity are positively correlated with bone loss and risk for fracture; however, after adjusting for confounding variables (eg, neuromuscular function, self-rated health status), this correlation did not always remain significant.10 The loss of statistical significance for the association of physical activity and bone mass in the older is probably that neuromuscular function is a mediator of physical activity and bone mass. Exercise can improve neuromuscular function and may reduce falls and fractures, more than increase bone mass and is critical to incorporate it into the treatment of osteoporosis to prevent fractures in the older.34 Furthermore, individuals with the TT genetic variant of the vitamin D receptor appear to be at a greater risk for this deleterious effect of caffeine on bone.34
Nutritional deficiency in dietary calcium intake is modestly correlated with BMD; however, many epidemiological studies of calcium intake and BMD in elders do not show a large impact on bone health implying other risk factors may be of greater importance in this age group.20 Nevertheless, age-related changes in bone strength are partly attributable to an increase in PTH secretion which in turn is related to low serum calcium and vitamin D levels.35
Intervention studies have revealed that calcium and vitamin D supplementation has a greater effect on serum PTH than either component alone.35 Furthermore, several lines of evidence suggest that vitamin D has a modest role in muscular strength and that supplementation improves muscle function, and body sway, and prevents falls.36,37
*Changes in Bone Architecture with Aging
*Approach to the Diagnosis of Bone Loss in the Aging Population
-Risk assessment/ dual-energy X-ray absorptiometry (DXA) and vertebral imaging
-Biochemical markers of bone turnover
-Use of WHO fracture risk assessment tool (FRAX)
*Approach to the Management of Bone Loss in the Older
-Vitamin supplementation
-Fall risk prevention and regular exercise
-Pharmacologic therapy
SUMMARY
Osteoporosis is the most common metabolic bone disease. With special respect to the older population, it is very common, not only due to changes in lifestyle and diet but as a result of the aging process, there is low-grade inflammation and immune system activation that directly affects bone strength and quality. A thorough screening for osteoporosis is needed to identify candidates for treatment. Treatment interventions focus on both non-pharmacologic (behavioral risk modification, diet, exercise, balance training) and pharmacologic (vitamin supplementation and medications). Careful screening and monitoring of older patients for bone health are critical to the prevention of fractures and obtaining a favorable outcome.
Review of Etiology, Mechanisms, and Approach to Management in the Aging Population (2023)
Sonali Khandelwal, MD,Nancy E. Lane, MD
Osteoporosis, the most common metabolic bone disease, is characterized by low bone mineral density (BMD) and reduced bone strength, and this results in an increased risk for fractures. It is a significant health problem, particularly affecting the aging population.
This article provides an update on the epidemiology, etiology, and approach to the diagnosis of osteoporosis in the aging population.
The prevalence of low bone mass and osteoporosis is high. An epidemiologic study determined that low femoral bone density is present in 14,646 US men and women from the Third National Health and Nutrition Examination Survey (NHANES III).1 According to the World Health Organization (WHO) criteria that use T scores (standard deviations below peak bone mass), this survey revealed that 13% to 18% of women aged 50 years or more had osteoporosis and another 37% to 50% had osteopenia. Applying these numbers to the most recent US census data in 2010 translates to over 10 million individuals with osteoporosis and over 20 million with osteopenia.1 Worldwide, approximately 200 million women have osteoporosis.2 Overall, the age-adjusted prevalence of osteoporosis among adults aged 50 and over has increased from 9.4% in 2007–2008 to 12.6% in 2017–2018. The prevalence of osteoporosis among women has increased from 14.0% in 2007–2008 to 19.6% in 2017–2018. However, osteoporosis prevalence in men did not significantly change from 2007–2008 (3.7%) to 2017–2018 (4.4%) (Fig. 1).
In the United States, 250,000 individuals aged 65 or greater fracture their hip each year.3–5 Hip fractures increase exponentially with age: the incidence of hip fractures in white women (per 1000 person-years) is 2.2, for ages 65 to 69 years; 4.4, for ages 70 to 74 years; 9.5, for ages 75–79 years; 16.9, age 80 to 84 years; 27.9, age 85 to 90 years; and 34.2, age 90 years and older.3,5 Hip fractures have long been considered one of the most devastating osteoporotic-related fractures due to postfracture disability and immobility. Unfortunately, hip fractures are projected to increase from an estimated 1.7 million in 1990 to 6.3 million by the year 2050.5,6 In addition, ethnic variations in bone mass have been noted in population studies.6 African Americans have higher and Asian Americans have lower BMD than White Americans.6 Moreover African Americans have lower fracture rates at many skeletal sites, including hip, clinical vertebral, upper, and lower appendages. In addition, Hispanic Americans and Asian Americans also have lower hip fracture rates than White Americans.6 In the United States for Caucasian ethnicity, it is currently estimated that the lifetime risk by age 50 of having a hip fracture is about 16% to 17.5% for women and 5% to 6% for men. For African Americans, the lifetime risk is lower but estimated to be 5.6% and 2.8% for women and men, respectively. Although the likelihood of developing osteoporosis is currently greatest in North America and Europe, as population longevity in developing countries increases so will the risk of osteoporosis.2
ETIOLOGY OF BONE LOSS IN AGING
Osteoporosis is a skeletal disorder characterized by compromised bone strength as well as bone quality predisposing to an increased risk of fractures. Normal bone remodeling involves an equilibrium between the process of bone resorption in which osteoclasts remove the bone by acidification and proteolytic digestion and bone formation in which osteoblasts secrete osteoid matrix into the resorption cavity.7 Activation of the remodeling cycle serves two functions in the adult skeleton (1) produce a supply of calcium to the extracellular space and (2) provide elasticity and strength to the skeleton. When the remodeling process is uncoupled there is either excess resorption of bone leading to bone loss versus excess bone acquisition when formation exceeds remodeling.8 In the bone remodeling process, osteoblasts are activated through various mechanisms including growth hormone, and parathyroid hormone (PTH). M-CSF and receptor activator of nuclear factor kappa-B ligand (RANKL) are the two major osteoblast-mediated factors, which regulate the recruitment of osteoclasts.7
In older individuals, there is an uncoupling of the bone remodeling cycle due to several factors, including a reduction in the number of activity of osteoblasts, so the amount of time to fill in resorption cavities is longer, and an increase in low-grade systemic inflammation, especially pro-inflammatory cytokines (TNF, IL-1, and IL-6) that seems to increase the number and activity of osteoclasts. Over time in older individuals, there is a net loss of bone. In addition to the uncoupling of bone remodeling with aging, the compromise of other major organs, such as the kidney reduces the activation of 25 D to 1.25 D which reduces the amount of calcium absorbed from the gastrointestinal tract, and a negative calcium balance ensues, and osteoclasts are required to resorb calcium to fill this gap.
In addition to uncoupling of normal bone homeostasis, inherent bone quality contributes to the risk of poor bone health. Small bone size, disrupted microarchitecture, cortical porosity, compromised quality of bone, and decreased viability of osteocytes are some biological factors contributing to decreased strength over time.8–10 A major determinant of bone density in an older individual is his or her peak bone mass.11,12 Peak bone mass is the maximum bone mass achieved in life. The time of peak bone mass is not known with certainty, but probably occurs in the third to fourth decade of life in most individuals, with differences in timing due to genetic, hormonal, and environmental variables and to the skeletal site (type of bone) and method of BMD measurement.11
In addition to the uncoupling of bone turnover, which is so common in aging, estrogen deficiency is also a critical factor for the development of osteoporosis in both women and men. Age-related bone loss may begin immediately after the acquisition of peak bone mass for either sex, however, most bone loss occurs after the age of menopause in women and after the age of 70 years in men.10 Nevertheless, it is unknown what contributes greater; to the molecular events causing disequilibrium between bone resorption and formation in aging versus sex steroid deficiencies.9 At menopause, there is a somewhat fast decline in ovarian function in women and a slower decline of both androgen and estrogen levels in men with advancing age, the two conditions inexorably overlap, making it impossible to separate their independent influence from the cumulative anatomic deficit.8 In Caucasian women aged 65 and older, both low serum total estradiol and high serum concentrations of sex hormone-binding globulin have been shown to increase the risk of hip and vertebral fractures without relation to BMD.10 Interestingly, mouse models of bone loss suggest that the adverse effects of old age on the skeleton are independent of estrogens and are due to molecular mechanisms that are distinct from those responsible for the effects of sex steroid deficiency.13–16
Suggested causes of bone-intrinsic molecular mechanisms include mitochondria dysfunction, oxidative stress, declining autophagy, DNA damage, osteoprogenitor, osteocyte senescence, senescence-associated secretory phenotype, and lipid peroxidation.14 Age-related changes in the bone resulting from intracellular reactive oxidative species (ROS) are not a new concept, but it has recently been proposed as a contributor to osteoporosis, especially in the older. ROS are generated during fatty acid oxidation and in response to inflammatory cytokines and it is suggested that both estrogens and androgens may protect against oxidative stress.15,16 In addition, estrogen withdrawal and deficiency at menopause are also believed to cause increased production of inflammatory cytokines and promote T-cell activation.17–19 The loss of estrogen results in the activation of specific T-cell subsets including T helper cells that support the production of IL-17, RANKL, IL-1, TNF, and IL-6 that stimulate osteoclast maturation, activity, and a lifespan that seem to prolong their lifespan and inhibit osteogenesis. In addition, estrogen deficiency and aging reduce the number and activity of Treg cells that reduce the production of inflammatory cytokines. These events that alter the immune system and inflammation with estrogen deficiency seem to increase with the addition of aging. Mouse models reveal the loss of estradiol due to ovariectomy increases osteoclast formation along with colony-forming units for granulocytes and macrophages in vitro. Similarly, this deficiency increases the number of osteoclasts in trabecular bone in animals. Along with elevated T cells, postmenopausal deficiency also stimulates B-lymphopoiesis. There has been a direct relationship observed between elevated B cells and bone resorption.
In addition to the normal aging process and menopause, there are many other clinical, medical, behavioral, and nutritional risk factors involved in the etiology of bone loss in the aging population.9 Clinical risk factors to consider include body mass. Older individuals with low body weight, low percentage of body fat, or low body mass index are at an increased risk of low bone mass and rapid bone loss.20 In addition, a history of prior fractures is extremely relevant as several studies have documented associations between prior fracture history at any site and risk of future vertebral and hip fractures and a first-degree relative having a history of a hip fracture.10,21–23 Moreover, in women who have developed an incident vertebral fracture, 1 in 5 develop a new incident vertebral fracture in the subsequent year.22 Impaired vision independently increases the risk of hip fracture in older white women10 and contributes to the risk for falls which is another independent risk factor for fracture. Finally, poor hand grip strength, a component of the definition of frailty, which can be caused by cognitive decline, diabetic neuropathy, or pain is a strong independent risk factor for fragility fractures in postmenopausal women.23
Several medical disorders as well as medications listed in Table 1 are associated with secondary osteoporosis in the aging population. This table albeit not fully inclusive of all conditions demonstrates the number of comorbidities that are highly prevalent in the older and can interfere with bone health. These disorders include gastrointestinal disorders (eg, inflammatory bowel disease, malabsorption syndromes, and celiac), hematologic disorders (eg, leukemia and lymphoma), endocrine disorders (eg, diabetes, hyperparathyroidism), and neurological disorders (eg, Parkinson’s disease, stroke), and renal insufficiency.24,25 In addition, exposure to certain medications may contribute to and/or increase the risk of bone loss. Glucocorticoids are the most implicated class of medication, affecting both bone quality and quantity of bone.26 Several studies investigating glucocorticoid-induced bone loss suggest that the degree of increased risk of vertebral fracture in glucocorticoid-treated men and women is disproportionate to observed decreases in BMD, leading investigators to surmise that in addition to reducing bone mass, glucocorticoid treatment may lead to bone quality defects mediated by increases in bone turnover and trabecular thinning.26,27 Other medications to consider are aromatase inhibitors, proton pump inhibitors, anticoagulants (heparin), selective serotonin reuptake inhibitors, and thiazolidinediones.
Behavioral factors have also been linked to the development of bone loss in older adults and include cigarette smoking, poor physical activity, and alcohol abuse. Cigarette smoking is believed to induce bone loss and increased hip fracture risk in the older part due to various mechanisms: (1) direct toxic effect on osteogenesis,28,29 (2) collagen metabolism in combination with increased bone resorption and osteoclast activity and osteoclastogenesis,30 (3) calciotropic hormone metabolism, (4) dysregulation of sex hormones,31 and (5) decreased intestinal calcium absorption.20,32,33 Some studies have suggested low levels of physical activity in the older, especially weight-bearing activity are positively correlated with bone loss and risk for fracture; however, after adjusting for confounding variables (eg, neuromuscular function, self-rated health status), this correlation did not always remain significant.10 The loss of statistical significance for the association of physical activity and bone mass in the older is probably that neuromuscular function is a mediator of physical activity and bone mass. Exercise can improve neuromuscular function and may reduce falls and fractures, more than increase bone mass and is critical to incorporate it into the treatment of osteoporosis to prevent fractures in the older.34 Furthermore, individuals with the TT genetic variant of the vitamin D receptor appear to be at a greater risk for this deleterious effect of caffeine on bone.34
Nutritional deficiency in dietary calcium intake is modestly correlated with BMD; however, many epidemiological studies of calcium intake and BMD in elders do not show a large impact on bone health implying other risk factors may be of greater importance in this age group.20 Nevertheless, age-related changes in bone strength are partly attributable to an increase in PTH secretion which in turn is related to low serum calcium and vitamin D levels.35
Intervention studies have revealed that calcium and vitamin D supplementation has a greater effect on serum PTH than either component alone.35 Furthermore, several lines of evidence suggest that vitamin D has a modest role in muscular strength and that supplementation improves muscle function, and body sway, and prevents falls.36,37
*Changes in Bone Architecture with Aging
*Approach to the Diagnosis of Bone Loss in the Aging Population
-Risk assessment/ dual-energy X-ray absorptiometry (DXA) and vertebral imaging
-Biochemical markers of bone turnover
-Use of WHO fracture risk assessment tool (FRAX)
*Approach to the Management of Bone Loss in the Older
-Vitamin supplementation
-Fall risk prevention and regular exercise
-Pharmacologic therapy
SUMMARY
Osteoporosis is the most common metabolic bone disease. With special respect to the older population, it is very common, not only due to changes in lifestyle and diet but as a result of the aging process, there is low-grade inflammation and immune system activation that directly affects bone strength and quality. A thorough screening for osteoporosis is needed to identify candidates for treatment. Treatment interventions focus on both non-pharmacologic (behavioral risk modification, diet, exercise, balance training) and pharmacologic (vitamin supplementation and medications). Careful screening and monitoring of older patients for bone health are critical to the prevention of fractures and obtaining a favorable outcome.
