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Osteoporosis

Introduction:
Osteoporosis is a metabolic bone disease that describes a reduction in bone mineral
density. The World Health Organization has defined osteoporosis as having a bone mineral
density (BMD) value greater than two standard deviations below the normal (average) bone
density of young white women (Porth 2009). The loss in bone density in this disease owns to
the increased risk of fractures due to bones becoming progressively more porous. The term
osteoporosis translates into porous bones, and it is the most common type of bone disease. In
fact, it is estimated that about 10 million Americans over the age of 50 currently have
osteoporosis and 34 million have low bone mass (osteopenia) and are at risk of developing the
disease (Porth 2009). It is also suggested that about half of all women and roughly a quarter of
all men older than the age of 50 will have broken a bone due to osteoporosis.
Osteoporosis is most common in post-menopausal women but also occurs in men and
increases in prevalence as ages increase. As a result, patients who suffer from osteoporosis
often experience reductions in quality of life, require long-term care, and have increased
mortality rates due their age and other possible complications or diseases (Curtis 2012).
Etiology and Pathophysiology:
The pathogenesis of osteoporosis is not fully understood, but research suggests that the
disease results from an imbalance in the rate of bone reabsorption and bone formation, referred
to as bone turnover or remodeling. Bone reabsorption periods during remodeling are faster than
bone reformation phase (Raisz 2005). As a result, an increase in the rate of bone turnover
causes a net loss of bone tissue as osteoclasts reabsorb more bone tissue than is formed by

osteoblasts over time. This loss of bone tissue contributes to the porous nature of bones in those
who suffer from osteoporosis (Lane 2006) (Walker 2008).
As one ages, the rates of bone remodeling fluctuates and affects bone development.
During childhood, bone mass increases steadily until it peaks in young adulthood. This is an
individuals peak bone mass density and it is an important determinant elderly bone density.
There are many factors that are associated with peak bone mass density and increased bone
turnover rates which may result in osteoporosis (Lane 2006). Genetic factors such as race and
gender have been linked to variances in peak BMD and turnover rates. For example, white and
Asian women have shown higher fracture rates than men at all ages, while black men have high
rates than women up until the age of 70. As previously mentioned, osteoporosis is a common
chronic disease of elderly populations and therefore age is considered to be among the top risk
factors for osteoporosis development among all genders and races (Lane 2006). Hormonal
factors also contribute to the possible development of osteoporosis later in life. Estrogen is an
important hormone for regulating bone formation and growth in both sexes. After menopause,
however, estrogen levels continuously decrease with age in women therefore contributing to an
increased rate of bone remodeling and a resulting net loss of bone tissue (Raisz 2005).
Behavioral and medical factors also play a role in the potential development of
secondary osteoporosis. Behavioral factors include modifiable risks such diet, exercise, and
smoking habits. Poor dietary calcium intake and vitamin D deficiencies, especially in the
elderly, are closely linked to reduced bone densities and increased remodeling rates as these are
important substances for bone health and development (Holick 2007). Smoking is also related
to accelerated bone loss due in part to reduced intestinal calcium absorption, while low levels
of physical activity, during adolescent bone growth in particular, is associated with low peak

bone mass density and an increased threat of osteoporosis development (Lane 2006).
Secondary osteoporosis can also result from medical factors. These risks include other diseases
such as gastrointestinal diseases, hematologic disease, and hypogonadal diseases, and exposure
to certain medications like glucocorticoids. These diseases and medications disrupt the bone
remodeling mechanism leading to a possible premature decrease in bone mass density or
heightened risk of osteoporosis development (Lane 2006) (Walker 2008).
Clinical Features and Diagnosis
Osteoporosis is a chronic disease that does not outwardly manifest itself with signs or
symptoms in early stages. The pathophysiology of the disease that leads to increased bone
turnover rates and therefore decreased bone densities causes bone fragility and susceptibility to
fracture (Kanis et al. 2008). As a result, people are quite often unaware they have osteoporosis
until a bone fracture occurs and they are informed by healthcare professionals. Common sites
of osteoporotic bone fractures include the vertebrae, hip, and the bones of the arms (Kanis et al.
2008).
Currently, osteoporosis is commonly diagnosed and monitored using bone mass density
measurements. As mentioned above, osteoporosis is defined as having a bone mass density of
at least two and a half standard deviations below the average bone density of young adult
women. There are several methods to measure BMD and properly diagnose osteoporosis. The
most common are imaging techniques that implement dual-energy X-ray absorptiometry,
ultrasound imaging, and quantitative CT scans (Kanis et al. 2008). Such techniques are used on
various parts of the skeleton and have individualized criterion used in diagnosing osteoporosis
and predicting fracture risks. However, factors other than BMD are associated with bone
fracture risks in people older than 60 years of age and those with co-morbidities. As a result,

the World Health Organization has developed the FRAX fracture risk assessment tool which
takes into account ones BMD levels and other clinical factors such as age, gender, and race in
order to quantify the risk of possible bone fracture within a 10 year period. However, the FRAX
tool does not provide intervention thresholds, the point at which intervention options are
appropriate (Curtis 2012). Such diagnostic and screening tools have proven to be successful in
reducing bone fracture recurrence in at-risk population after initial bone fracture (Davis 2010).
Along with BMD screening and fracture risk assessments, it is recommended that patients
should also be screened for risk factors that contribute to secondary osteoporosis such as
lifestyle behaviors, family history and other medical complications.
Treatment and Prevention
With regards to osteoporosis, treatments are implemented to reduce the morbidity and
mortality of bone fractures and bone tissue loss due to osteoporosis. Of the recommended
therapies, lifestyle modifications are the most commonly ascribed management options for
those with osteoporosis. Such modifications include smoking cessation, weight-bearing
physical activity, and dietary changes that permit proper calcium and vitamin D consumption
(Davis 2010) (Holick 2007). Fall risk assessments and preventative measures are also
implemented in a clinical setting to prevent possible fractures from falling and future fall risks
(Elliot 2010).
Along with lifestyle modifications, drug therapies have been developed and have
proven to be effective in osteoporosis management. Antiresorptive drugs that are purposed to
reduce bone reabsorption rates include bisphosphonates, calcitonin, and estrogen-replacement
therapies (Davis 2010). Bisphosphonates, however, have come under recent scrutiny despite
being highly effective in preventing recurring osteoporotic fractures (Whitaker et al 2012). For

example, zoledronic acid is a bisphosphonate commonly used in osteoporosis management that


has been highly effective in preventing both vertebral and nonvertebral fractures but lacks
established long-term safety and efficacy information (Boonen et al 2010). Such medications
are still being studied in order to elucidate long-term safety effects and optimal therapy
durations for maintaining protection against bone fractures (Whitaker et al. 2012). Another
class of drug is anabolic agents. Such therapy, which includes a form of parathyroid hormone
called teriparatide, maintains ones BMD by causing bone tissue production (Davis 2010).
Furthermore, as previously mentioned, diagnostic screening of ones bone mass density
and fracture risk assessment are methods developed in order to diagnose osteoporosis. Such
techniques are also implemented along with lifestyle and drug therapies to prevent and control
the risk of osteoporotic fractures in elderly patients and other high-risk populations. Early
detection and prevention are crucial for managing osteoporosis and improving a patients
quality of life.

Works Cited
Boonen, S., Black, D. M., Coln-Emeric, C. S., Eastell, R., Magaziner, J. S., Eriksen, E. F., Lyles,
K. W. (2010). Efficacy and safety of a once-yearly intravenous zoledronic acid 5 mg for
fracture prevention in elderly postmenopausal women with osteoporosis aged 75 and older.
Journal Of The American Geriatrics Society, 58(2), 292299. doi:10.1111/j.15325415.2009.02673.x
Curtis, J. R., & Safford, M. M. (2012). Management of osteoporosis among the elderly with other
chronic medical conditions. Drugs & Aging, 29(7), 549564. doi:10.2165/11599620000000000-00000
Davis. (2010, June 7). Approved Treatments for Osteoporosis and Whats in the Pipeline - Drug
Benefit Trends. Retrieved March 6, 2013, from
http://dbt.consultantlive.com/display/article/1145628/1583209
Elliott, M. (2011). Taking control of osteoporosis to cut down on risk of fracture. Nursing Older
People, 23(3), 3035.
Holick, M. F. (2007). Optimal vitamin D status for the prevention and treatment of osteoporosis.
Drugs & Aging, 24(12), 10171029.
Kanis, J. A., Burlet, N., Cooper, C., Delmas, P. D., Reginster, J.-Y., Borgstrom, F., & Rizzoli, R.
(2008). European guidance for the diagnosis and management of osteoporosis in
postmenopausal women. Osteoporosis International, 19(4), 399428. doi:10.1007/s00198-0080560-z
Lane, N. (2006). Epidemiology, etiology, and diagnosis of osteoporosis. American Journal of
Obstetrics and Gynecology, (194), S311.
Porth, C., & Matfin, G. (2009). Pathophysiology (8th ed.). Wolters Kluwer Health.

Raisz, L. G. (2005). Pathogenesis of osteoporosis: concepts, conflicts, and prospects. Journal of


Clinical Investigation, 115(12), 33183325. doi:10.1172/JCI27071
Walker, J. (2008). Osteoporosis: pathogenesis, diagnosis and management. Nursing Standard (Royal
College Of Nursing (Great Britain): 1987), 22(17), 4856.
Whitaker, M., Guo, J., Kehoe, T., & Benson, G. (2012). Bisphosphonates for Osteoporosis Where
Do We Go from Here? New England Journal of Medicine, 366(22), 20482051.
doi:10.1056/NEJMp1202619

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