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Stephanie Fenton

NDFS 356
March 17, 2016
OSTEOPOROSIS
Introduction
Osteoporosis is a chronic disease that affects the skeleton, primarily in the elderly (1). It
is defined by the World Health Organization as a systemic skeletal disease characterized by low
bone mass and microarchitectural deterioration of bone tissue with a consequent increase in bone
fragility and susceptibility to fracture (2). As stated in this definition, progression of the disease
can eventually lead to an increased risk of fractures, especially in the hip, which results in
increased rates of morbidity and mortality in osteoporotic patients (3). There are several ways to
diagnose and treat the disease once it has begun to deteriorate the bones.
Disease Description
WHO further defines osteoporosis as the point when bone mineral density (BMD)
reaches 2.5 or more standard deviations below peak bone mass (PBM), to the point where the
human skeleton is no longer able to withstand small strains, such as tripping over a stair or
falling to the floor. Before an individual reaches this point, they may be diagnosed with
osteopenia, if they have a BMD 1 standard deviation below PBM. Unfortunately, once a person
develops one of these conditions, there is no cure. However, there are ways to slow the
development of osteoporosis, or more importantly, prevent it before it starts (1).
Whether as a result of low nutrient intake or physical activity during growth, or lesscontrollable factors such as genes, some people do not reach an optimal PBM, or they experience
excessive breakdown of bone in their later years. Currently, about eight million women and two

million men have osteoporosis in the United States, and in 2005 there were more than two
million fractures from osteoporosis (1).
It is important to first understand the structure and development of bone before delving
into the details of the diseases it is affected by. Bone is made of osteoid, which is primarily
composed of collagen fibers in which calcium and phosphate salts are combined with
hydroxyapatite crystals to form the sturdy matrix that supports most of our body weight. There
are two types of bone: cortical and trabecular. Cortical makes up the shafts of long bones, while
trabecular can be found in the ends of bones and is also known as spongy bone, due to its
porous structure (1).
Pathophysiology
During ones lifetime, bone is being constantly remodeled. Cells called osteoblasts are
responsible for forming new bone, while osteoclasts are degrading and reabsorbing it. The
calcium found in bone is also present in the blood to a much smaller degree, and several
hormones play a role in regulating the amount of calcium in bone and blood, including
parathyroid hormone and calcitonin. During growth of the skeleton, bone mass increases until
peak bone mass is reached around age 30. Around age 40, osteoclast activity is greater than that
of osteoblasts, and bone begins to disappear more quickly than it is rebuilt. Bone mineral content
(BMC) measures bone accumulation before PMB is reached, while bone mineral density (BMD)
refers to bone mass after the bones stop growing. Since osteoporosis occurs mainly in the elderly,
BMD is evaluated more frequently than BMC in nutritional assessment for the disease (1).

Etiology, Risk Factors, and Prevention

Because PBM is reached around age 30, it is vital for individuals to take proper measures
to reach optimal PBM during the years of bone growth and maturation. While kids are growing,
it is important that they consume adequate calcium for bone structure, and vitamin D, which
assists calcium in building and strengthening the skeleton. Adequate calories and protein,
combined with an overall healthy diet will decrease the risk of obtaining sub-optimal PBM,
which could result in weaker bones in later years (1).
Osteoblast and osteoclast activity respond to pressure put on bones. Weight-bearing
exercise, such as running and weightlifting increase activity of osteoblasts, thus increasing bone
mass. During development, it is important for individuals to live active lifestyles and exercise
regularly to improve PBM. Even in older individuals, exercise reduces skeletal inflammatory
markers and stimulates osteoblast function, which can slow loss of bone (1). Strength-training
has also been found to reduce the risk of fractures and improve BMD in postmenopausal women
(4).
Studies have found that lean body mass exerts a greater force on bone than fat mass (5).
Thus, it is important to participate in strength-training exercises to increase lean body mass and
subsequently improve BMD. In addition, fat mass increases inflammatory responses which is
detrimental to bone because it stimulates osteoclast activity (6).
It is important to reduce the risk of fractures after being diagnosed with osteoporosis, due
to increased fragility of the bones. Aside from finding treatment to slow progression of the
disease, the environment of the patient should be altered to provide safety and stability. For
example, the home should be well lit and floors should be slip-resistant. Grab rails may be
installed in the shower as well as chairs or stools for the patient to sit in while bathing. Tripping
hazards such as cords and loose rugs should be kept free from any walkway (7).

Studies have shown that low phytate intake may be a risk factor for osteoporosis, because
it has been associated with a lower bone mineral density. Phytates are naturally-occurring
compounds found in fiber-rich foods such as whole grains. Increasing consumption of whole
wheat breads and bread products is one way to increase phytate intake and thus decrease risk of
osteoporosis (8).
Alcohol intake and cigarette use increase the risk of osteoporosis due to their toxic effect
on osteoblasts. Moderate alcohol intake may, in fact, present a positive effect in postmenopausal
women. However, excessive alcohol intake is likely to cause bone loss, and the combination of
smoking and alcohol further increases the risk of osteoporosis (1). Calcium may exert a negative
impact on bone density due to its effect on cyclic AMP, which in turn increases parathyroid
hormone-mediated bone resorption. However, studies have been inconclusive in this regard. In
human studies, intake of caffeinated beverages appears to have little effect on BMD unless
combined with smoking and/or alcohol use (9). Having a low body weight is a risk factor for
osteoporosis, because there is less pressure placed on the skeleton, so bone is not built as dense
and strong. Whites and Asians have more osteoporotic fractures, while Blacks and Hispanics
tend to have greater bone density. Some medications may interfere with calcium absorption or
promote calcium loss from bone (1).
Osteoporosis has a strong genetic component. It is a polygenic disorder, thus influenced
by mutations in several genes. In studies of twins, inheritability of BMD has been found to lie
between 50% and 85%. Several predictors of fracture risk have a heritable component including:
hip axis length, ultrasound properties of bone, body mass index, muscle strength, and age at
menopause. Patterns of inheritance vary widely among families; however it is possible to

determine severity of osteoporosis risk by examining the number of mutated genes regulating
bone mass and health (10).
For women, lactation causes bone loss due to loss of calcium. It is vital for mothers to
consume adequate vitamin D and calcium during lactation to prevent extensive bone loss. Later
in life, menopause causes a reduction in estrogen production, which results in an increase in
osteoclast activity (1). Osteoclast numbers also rise due to both increased formation and
decreased apoptosis of old cells. Estrogen down-regulates pro-inflammatory cytokines such as
IL-1, IL-6, and granulocyte macrophage colony-stimulating factor, which increase bone
resorption (11). Amenorrhea in younger women is also associated with bone loss due to
decreased estrogen circulating the body (1).
There are two different types of osteoporosis: primary and secondary. Primary is divided
into two sub categories. The first is estrogen-androgen deficient osteoporosis, in which a
decrease in estrogen (due to menopause in women) or decrease in androgens in men lowers bone
density. In men, this condition is very rare and is typically accompanied by fractures of the distal
radius and crush fractures in the lumbar vertebrae. Age-related osteoporosis affects women
more than men (due to lesser skeletal mass) and increases the risk of fractures, especially hip
fractures. Secondary osteoporosis occurs when drugs or disease cause a loss of bone tissue (1).
Some categories of secondary osteoporosis include: chronic and systemic diseases (amyloidosis,
multiple myeloma, renal failure, etc.), endocrine and metabolic disorders (type 1 diabetes,
hyperthyroidism, hemochromatosis, etc.), medications (glucocorticoids, heparin, lithium, etc.),
and poor nutrition (alcohol, celiac disease, anorexia nervosa, etc.) (3).

Methods of Medical Diagnosis

There are several ways to test for osteoporosis, and early diagnosis is key to successful
treatment. As of 2013, X-ray absorptiometry was the most commonly used method for measuring
bone density. However, this method is very costly and delivers high doses of radiation.
Researchers have further noted that in order to properly assess fracture risk, mechanical features
and elastic properties of bone need to be measure, which cannot be done using X-ray.
Quantitative ultrasound (QUS) is capable of obtaining these additional measures, but testing is
limited by the fact that QUS can only be used to measure the peripheral skeleton (2). DXA (dual
x-ray absorptiometry) scans remain a commonly used measurement tool today. Scans are
typically completed of the hip and spine to assess bone density. FRAX is an assessment tool that
examines bone density and other risk factors to determine fracture risk in elderly patients and
people with osteopenia or osteoporosis (12).
Current Medical Therapies
There is no cure to osteoporosis; however, the progress of the disease can be slowed and
symptoms can be treated with a variety of medical therapies. One of the first therapies prescribed
to postmenopausal women and men with high fracture risk is parathyroid hormone (PTH)
therapy, which functions by increasing osteoblast number and function, which in turn increases
total body BMD. Estrogen replacement therapy is used for postmenopausal women to negate the
effects of reduced estrogen release (1). However, such therapy may result in severe side effects
such as: heart attack, stroke, blood clotting, and increased risk of breast and endometrial cancer
(13). Bisphosphonates limit the activity of osteoclasts, thus slowing bone resorption and reducing
the risk of fractures. Possible side effects include gastrointestinal problems and jaw necrosis,
which is fairly rare. Calcitonin is sometimes administered to limit the stimulatory effect of PTH

on osteoclasts. Selective estrogen receptor modulators (SERMs) are used to stimulate estrogen
receptors in bone tissue (1).
Several alternative and complementary therapies have been indicated for treatment of
osteoporosis, including plant-based supplements. Such supplements are not closely regulated by
the FDA, and patients should talk to their doctors before considering use. Onion is thought to
decrease bone resorption and increase bone mineral content, and garlic has been shown to
decrease bone loss in rats. Green tea tends to increase estrogen and bone formation in rats, but
human studies are limited. Other plant-based alternative therapies for treating osteoporosis
include: soy, safflower, olive, sage, thyme, flowering okra, juniper, pine, prune, tomatoes, black
cohosh, and several others (13).
Nutrition Assessment Tools
In assessing an individual with osteoporosis, it is important to periodically look at bone
density to assess progression of bone loss and determine further course of action. Dietary history
and risk factors should be reviewed to determine what might be the underlying cause of the
disease and correct any nutrient deficiencies. The dietitian should also measure the patients
height (which typically decreases over time in osteoporotic patients) and determine activity level
and amount of weight-bearing exercise being performed (1). Questions should be asked
regarding the patients history of broken bones, smoking or drinking habits, history of eating
disorders or amenorrhea, current medications, and family history of osteoporosis (12).
Laboratory tests can be completed to determine the cause of bone loss if cause is
secondary. Lab values assessed include: blood calcium levels, thyroid function tests, parathyroid
hormone levels, testosterone levels, and biochemical marker tests. It can be helpful to know if
any of these lab values are out of the normal range so the underlying cause can be treated (12).

MNT
After assessment, treatment may include the following: calcium supplementation (1000
mg/day) and/or vitamin D supplementation (800-1000 units/day) to reduce risk of fracture and
improve BMD. It is important to make sure the osteoporotic patient is consuming adequate
calories and protein to support bone and supply adequate nutrition (1). The dietitian should
assess the patients current dietary needs and suggest foods that fit with their lifestyle and
possible allergies. For example, if a patient is lactose intolerant, the dietitian could recommend
consumption of calcium and vitamin D fortified milk replacements such as almond milk or soy
milk (14).
Many osteoporosis patients are underweight due to decreased lean body mass and fat
stores. If this is the case, a diet with adequate calories for weight gain should be recommended.
The Mifflin equation can be used to estimate energy requirements. It is a good idea to obtain a
history of the patients weight to determine severity of weight loss, especially because
underweight is associated with increased rates of mortality in older adults (14).
Conclusion
Though there are several ways to define osteoporosis, it can be simply described as a
chronic disease resulting in slow deterioration of bone. It is incurable once it starts; however,
progression can be slowed, and some bone mass may be regained with proper treatment.
Preferably, the disease should be prevented altogether by consuming a diet with adequate
calories, proteins, vitamins, and minerals, especially calcium and vitamin D which are vital to the
growth and structure of bone. Weight-bearing exercise is important to develop strong PBM and
limit cytokine-secreting adipose tissue. Once someone develops osteoporosis, medications,
exercises, and vitamin supplements may help slow the course of the disease. There are many

alternative and complementary therapies suggested for treatment of the disease, however a
patient should talk to their doctor before considering their use. Finally, it is important to protect
an osteoporotic patient against the risk of fractures, especially hip fractures, by modifying the
living/home environment to prevent falls.

References
1. Mahan KL, Escot-Stump S, Raymond JL. Krauses Food and the Nutrition Care Process.
13th ed. St. Louis: Elsevier Saunders; 2012.
2. Pisani P, Renna MD, Conversano F, et al. Screening and early diagnosis of osteoporosis
through X-ray and ultrasound based techniques. World J Radiol. 2013;5(11):398-410.
3. American Family Physician. Diagnosis and treatment of osteoporosis. Available at:
http://www.aafp.org/afp/2009/0201/p193.html. Accessed March 16, 2016.
4. Howe TE, Shea B, Dawson LJ, et al. Exercise for preventing and treating osteoporosis in
postmenopausal women. Cochrane Database Syst Rev. 2011;(7):CD000333.
5. Ho-Pham LT, Nguyen UD, Nguyen TV. Association between lean mass, fat mass, and
bone mineral density: a meta-analysis. Clin Endocrinol Metab. 2014;99(1):30-38.
6. Cao JJ. Effects of obesity on bone metabolism. J Orthop Surg Res. 2011;6:30.
7. NIH Osteoporosis and Related Bone Diseases National Resource Center. Once is enough:
a guide to prevening future fractures. Available at:
http://www.niams.nih.gov/Health_Info/bone/Osteoporosis/Fracture/default.asp. Accessed
March 16, 2016.
8. Lpez-Gonzlez AA, Grases F, Roca P, Mari B, Vicente-Herrero MT, Costa-Bauz.
Phytate (myo-inositol hexaphosphate) and risk factors for osteoporosis. J Med Food.
2008;11:747-752.
9. Cooper C, Atkinson EJ, Wahner HW, et al. Is caffeine consumption a risk factor for
osteoporosis? J Bone Miner Res. 1992;7:465-471.
10. Stewart TL, Ralston SH. Role of genetic factors in the pathogenesis of osteoporosis. J
Endocrinol. 2000;166(2):235-245.
11. Riggs BL. The mechanisms of estrogen regulation of bone resorption. J Clin Invest.
2000;106:1203-1204.
12. National Osteoporosis Foundation. Making a diagnosis. Available at:
http://nof.org/articles/8. Accessed March 16, 2016.
13. Banu J, Varela E, Fernandes G. Alternative therapies for the prevention and treatment of
osteoporosis. Nutr Rev. 2012;70(1):22-40.
14. Packard PT, Heaney RP. Medical nutrition therapy for patients with osteoporosis. J Am
Diet Assoc. 1997;97:414-417.

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