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POSTMENOPAUSAL OSTEOPOROSIS
It has been calculated that, at the time of
peak height velocity (12–13 years in females and
14–15 years in males; pubertal stages 2 and 3),
the percentage total height gain is greater than
the percentage incremental areal BMD at the
lumbar spine, femoral neck and femoral mid-
shaft. In males, the greatest difference between
height and BMD gains is more pronounced at
the lumbar spine and femoral neck than at the
femoral mid-shaft, whereas in females the differ-
ence appears to be of a lower magnitude than in
males
10
. Moreover, Theintz and colleagues
4
demonstrated that the increment in bone mass at
the lumbar spine as a function of height gain fol-
lows a loop pattern when pubertal stages are
taken into consideration. The model suggests
that there is a dissociation between the incre-
ment of bone mass and height gain; in the last
stages of puberty, when height gain decreases
abruptly, bone mass accumulation is sustained.
Therefore, an accumulation of lumbar bone mass
occurs after the attainment of peak height veloc-
ity in both sexes.
DETERMINANTS OF PEAK BONE
MASS
Many factors, more or less independent, are
known to influence the acquisition of bone mass
during childhood and adolescence. These deter-
minants include both endogenous and exogenous
factors. Furthermore, some diseases may affect,
per se or by their treatment, the acquisition of
bone mass in children and adolescents
16
.
Genetic factors
The main determinant of PBM appears to be
genetic factors. Indeed, twin and family studies
support a strong genetic component of BMD,
accounting for approximately 70–80% of adult
BMD
17–21
. Most studies have used methods that
identify candidate genes which could be involved
in the regulation of bone turnover, or polymor-
phisms for these genes. The involved genes are
not clearly identified, but the most important are
probably those related to body size
22
. It has been
suggested that a polymorphism in the vitamin D
Table 1 Some genetic determinants of bone mass
Vitamin D receptor (VDR)
Estradiol receptor (ER)
Calcitonin receptor (CTR)
Calcium-sensing receptor (CASR)
Glucocorticoid receptor (GR)
Parathyroid hormone
Transforming growth factor
β1 (TGF
β
1)
Interleukin-6 (IL-6)
Insulin-like growth factor-I (IGF-I)
Collagen type I
a1
(COL1A1)
Osteocalcin (BGP)
receptor gene (VDR) may be an important deter-
minant of bone mass
23
. However, conflicting
data have been reported in both adults
24,25
and
children
26–30
regarding the association between
VDR polymorphism and BMD values or predis-
position to osteoporosis. Some genetic determi-
nants of bone mass have been identified (Table
1), but their predictive role in children at risk of
osteoporosis is not defined. The mechanism(s) by
which the genetic factors determine BMD is
unknown, but lean and fat mass, body weight,
muscle strength, hormone secretion, timing of
puberty and even physical and dietary tendencies
may be influenced by hereditary factors.
However, it is important to consider that
heredity and environment are not separable.
Indeed, genetic factors could influence the effi-
ciency with which an individual utilizes and con-
serves the nutrients needed for the acquisition of
bone mass
22
. Moreover, some environmental fac-
tors may have different effects due to different
expression of a genetic determinant.
Regarding racial factors, BMD values are
higher in black than in white subjects, and lower
in girls of Asian ethnicity than in Caucasian
girls
7
.
Hormones
Many hormones are involved in the acquisition of
bone mass: sex steroids, the growth hormone
(GH)–insulin-like growth factor-I (IGF-I) axis,
1,25-dihydroxyvitamin D (1,25(OH)
2
D), thy-
roid hormones, insulin, glucocorticoids, parathy-
64
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BONE MINERAL ACQUISITION DURING INFANCY AND ADOLESCENCE
roid hormone and calcitonin
9
. Some clinical evi-
dence in patients with altered hormonal secretion
suggested that sex steroids and the GH–IGF-I
axis play a main role in the acquisition of bone
mass
16,31,32
. Indeed, individuals with mutations
of the estrogen receptor and aromatase genes
have estrogen deficiency and osteoporosis
16,31,32
.
The predominant effect of testosterone on bone
mass accumulation occurs via its aromatization
to estrogen, but it may cause indirect effects via
its anabolic action on lean tissue mass and a weak
direct effect via its action on osteoblasts
32
. Chil-
dren with GH deficiency have reduced bone
turnover and BMD, but long-term GH therapy
is able to improve both
16
. The role of sex steroids
and the GH–IGF-I axis in the acquisition of
bone mass is mainly evident during puberty,
when the gain of bone mass is maximal.
Balance studies showed that the percentage of
intestinal calcium absorption is closely related to
circulating 1,25(OH)
2
D concentrations. Indeed,
intestinal calcium absorption is approximately
40% when 1,25(OH)
2
D levels are in the normal
range, but it may be extremely low (< 10%)
if 1,25(OH)
2
D levels are reduced. Therefore,
an optimal vitamin D status is a key factor in
regulating intestinal calcium absorption
33
.
Dietary calcium
Relationships between calcium intake and adult
BMD have been reported from many cross-
sectional and retrospective studies; however,
other studies did not show this association
22,34–37
.
Some meta-analyses have concluded that calcium
intake is a significant determinant of BMD but
the magnitude of the effect is probably small, at
about 1% of the population variance
36
. At any
rate, there is evidence that a reduced calcium
intake may be associated with a low bone mass
and fractures in children
38
and adolescents
39–41
.
Moreover, it has been shown that women with a
low calcium intake during childhood and adoles-
cence have less bone mass in adulthood and a
greater risk of fracture
42
.
On the other hand, studies of calcium supple-
mentation showed that a calcium intake above
the recommended intakes was able to improve
the accumulation of bone mass in prepubertal
and pubertal healthy subjects
1–3
. The mecha-
nism(s) by which calcium supplementation pro-
duces its effect is probably related to a reduced
bone turnover, stimulating the acquisition of
bone mass
43
. However, subsequent studies
reported that the effect of calcium supplementa-
tion on BMD ceased after the discontinuation of
supplementation
44,45
, whereas others showed a
persisting effect of calcium supplementation on
BMD until 3–5 years after the end of interven-
tion
46
. A longer period of calcium supplementa-
tion, up to the attainment of PBM, will give
more information on the long-term effect of cal-
cium intake on bone mass.
Exposure to risk factors such as excessive
sodium, phosphate, animal protein, caffeine and
alcohol intakes may affect the accumulation of
bone mass
47
.
Physical exercise
The role of physical exercise in the development
and maintenance of skeletal mass is generally
accepted, but the data are not univocal. This is
due to the difficulty in quantifying the effect of
physical exercise alone, independently of the
other determinants of PBM. In adults, physical
activity is associated with greater bone mass
48
.
The dominant arm in tennis players has greater
bone mass than the non-dominant arm
49
. In con-
trast, complete (e.g. prolonged bed-rest, space-
flight, traumatic paraplegia, cerebral palsy) or
partial immobilization (e.g. fractures) was shown
to result in various degrees of bone loss
50,51
, but
bone formation dramatically increased when
immobilized subjects resumed exercise
52
.
Few studies of the effect of physical exercise
on BMD have been performed in children or
adolescents. It has been shown that weight-bear-
ing exercises during, and to a lesser extent after,
puberty may improve BMD, mainly at the hip
32
.
Non-weight-bearing exercises, such as swim-
ming, did not increase BMD
32
. Ruiz and col-
leagues
53
also demonstrated that physical activ-
ity was strongly correlated with lumbar BMD;
the correlation was present both during the ini-
tial phase of puberty (Tanner stage 2) and during
puberty (Tanner stages 4–5). Moreover, Nord-
strom and associates
54
demonstrated that BMD
65
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POSTMENOPAUSAL OSTEOPOROSIS
(measured for total body, head, humerus, spine,
femur and tibia/fibula) was significantly corre-
lated with muscle strength measured at the
quadriceps. These results confirm previous data
showing a correlation of muscle strength in the
back with BMD of the lumbar spine
55
, and of
grip strength with BMD at the mid-radius
56
.
Furthermore, a study by Schonau
57
at the distal
radius, using peripheral quantitative computed
tomography, showed that parameters of bone
geometry such as bone cross-sectional area and
cortical area, and bone strength index (which
derives from the section modulus and the volu-
metric density of the cortical area), were corre-
lated with grip strength measured by hand
dynamometer.
Regular weight-bearing activity probably has
a greater influence on bone mass than dietary
calcium
58
. In any case, physical activity and cal-
cium intake may not act on bone independent of
each other. Indeed, a positive effect of physical
activity appeared only at calcium intakes greater
than 1000 mg/day, and the beneficial effect of a
high calcium intake appeared only when physical
activity was carried out
59
. Regarding the inter-
action between genetic and environmental fac-
tors and the acquisition of bone mass, an inter-
esting hypothesis has been suggested by Kelly
and colleagues
60
: with low calcium intake or low
physical activity there is little difference between
subjects with high or low genetic potential.
Therefore, in order to obtain maximal expres-
sion of the genetic potential to achieve PBM,
association of a high dietary calcium intake and
regular physical activity is necessary.
CONCLUSIONS AND
RECOMMENDATIONS
(1) Peak bone mass (PBM) is attained during
late adolescence, and puberty represents a
critical period for bone mass accumulation.
(2) PBM is the result of the interaction of vari-
ous factors: genetic, hormonal, racial, nutri-
tional, life-style and physical exercise.
(3) Environmental factors modulate the expres-
sion of the genetic potential to achieve PBM.
(4) Calcium intake seems to be a main nutri-
tional determinant in bone mass acquisition.
In children and adolescents in whom cal-
cium intake is deficient, calcium supple-
mentation according to adequate intake for
age is recommended.
(5) Vitamin D has a major role in stimulating
intestinal calcium absorption. In children
and adolescents having an insufficient vita-
min D status, vitamin D supplementation
according to adequate intake for age is
recommended.
(6) Physical exercise (mainly regular weight-
bearing activity) is a key factor for the
acquisition and maintenance of bone mass.
66
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Osteoporosis: influence of life-style
R. Rizzoli
9
71
INTRODUCTION
Diagnosis of the disease relies on the quantitative
assessment of bone mineral mass/density, which
represents one major determinant of bone
strength and, thereby, of fracture risk. However,
indications for treatment are based on the evalu-
ation of fracture risk, which also integrates other
factors, clinical and biochemical, compared with
osteoporosis diagnosis. The age-related increase
in fracture risk depends on a progressive decrease
in bone mass, and a rising risk of falling. How-
ever, a minority of falls in the elderly (less than
2%) result in hip fracture
1
. The incidence of
osteoporotic fractures varies from region to
region, and may be related to population age dis-
tribution, genetic background or life-style condi-
tions. For instance, it appears that hip fracture
incidence is higher in urban than in rural areas in
a given population
2
. Up to 40% of hip fractures
concern patients living in nursing-homes
3
. This
is probably related to advanced age and to a high
prevalence of comorbidities requiring long-term
care.
EXTRASKELETAL DETERMINANTS
OF OSTEOPOROTIC FRACTURES
Almost all fractures, even those qualifying as
‘low trauma’ fractures, occur as a result of some
injury. Usually this is the result of a fall, or the
application of a specific loading event in some
cases of vertebral fracture, such as bending for-
ward to lift a heavy object with the arms
extended. The risk of falling increases with age.
Most falls in the elderly are due to intrinsic and
extrinsic or environmental factors (Table 1).
Among the intrinsic factors, the risk of falling
increases with the number of disabilities. Impair-
Table 1 Risk factors associated with falls. Adapted
from reference 4
Impaired mobility, disability
Impaired gait and balance
Neuromuscular or musculoskeletal disorders
Age
Impaired vision
Neurological, heart disorders
History of falls
Medication
Cognitive impairment
ment of gait, mobility and balance are the most
consistently identified risk factors for falls and
fall-related injuries. The ability to maintain pos-
tural control and avoid environmental obstacles
depends on proprioceptive, vestibular and visual
input translated into appropriate motor
responses. Thus, the risk of falling increases with
reduced visual acuity or diminished sensory per-
ception of the lower extremities. Chronic ill-
nesses, such as various neurological disorders,
heart diseases, stroke, urinary incontinence,
depression and impaired cognitive functions,
increase the risk of falling. Medications such as
hypnotics, antidepressants or sedatives are associ-
ated with falls. Environmental factors include
potential hazards that can be found in the home,
such as slippery floors, unstable furniture or
insufficient lighting. The orientation of falls
influences the consequences of falling. Indeed,
the points of impact of a fall determine the type
and extent of injury. When falling, the elderly
tend to land on the hip. In contrast, middle-aged
adults tend to fall forward, with the main impact
on the wrist. Several reflexes and postural
responses are initiated during a fall which can
prevent or reduce the injury. The effectiveness of
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reflex actions depends on the speed of execution
and the strength of the muscles initiating the
protective movement. The impact of falls can be
absorbed by surrounding soft tissue. The appar-
ent protective effect of higher body weight may
be due, at least in part, to the local shock-
absorbing capacity of muscle and fat.
RISK FACTORS
Risk factors for osteoporotic fractures are listed in
Table 2. The onset of substantial bone loss occurs
at the age of 50 and 65 years in women and men,
respectively. In contrast with bone mineral
accrual during adolescence, bone size varies little
throughout life, beyond the continuous and
slight expansion of bone outer dimensions, which
is mainly found in men, and which affects both
the axial and the peripheral skeleton. This
periosteal expansion is less than the increase in
bone marrow space, which results from continu-
ous endosteal resorption. Under these conditions,
bone cortex becomes thinner. This phenomenon,
together with an increment in cortical porosity
and the destruction of trabeculae through thin-
ning and perforation, accounts for age-depend-
ent bone loss. Thus, this modeling process could
be interpreted as a response to bone loss, in an
attempt to compensate for a reduction in
mechanical resistance
6
.
Nutritional causes of bone mass loss
Calcium intake, vitamin D and osteoporosis
Calcium contributes to preservation of the bony
tissue during adulthood, particularly in the eld-
erly. Without an appropriate supply of vitamin
D, from cutaneous and/or exogenous sources, the
bioavailability and metabolism of calcium are
disturbed
7
. This results in accelerated bone loss.
In the elderly, several alterations contribute
towards a negative calcium balance. Indeed, with
aging there is a decrease in calcium intake
because of a reduction in dairy products
consumption, in intestinal absorption of calcium,
in the absorptive capacity of the intestinal
epithelium to adapt to a low calcium intake, in
72
Table 2 Risk factors for osteoporotic fractures.
Adapted from reference 5
Female sex
Premature menopause
Age
*
Primary or secondary amenorrhea
Primary and secondary hypogonadism in men
Asian or white ethnic origin
Previous fragility fracture
*
Low bone mineral density
Glucocorticoid therapy
*
High bone turnover
*
Family history of hip fracture
*
Poor visual acuity
*
Low body weight
*
Neuromuscular disorders
*
Cigarette smoking
*
Excessive alcohol consumption
Long-term immobilization
Low dietary calcium intake
Vitamin D deficiency
*
Characteristics that capture aspects of fracture risk
over and above that provided by bone mineral density
POSTMENOPAUSAL OSTEOPOROSIS
exposure to sunlight and the capacity of the skin
to produce vitamin D, and in renal reabsorption
of calcium; there is also a decrease in the tubular
calcium reabsorptive capacity to respond to the
stimulatory effect of parathyroid hormone
(PTH). Furthermore, the mild renal insufficiency
regularly observed in the elderly can contribute
to a state of chronic hyperparathyroidism that
favors negative bone mineral balance and
thereby osteoporosis. Increasing the calcium
intake is certainly an important strategy, which
appears to be relatively easier to implement com-
pared with other possible preventive measures.
Protein malnutrition
Nutritional deficiencies play a significant role in
osteoporosis in the elderly. Indeed, undernutri-
tion is often observed in the elderly, and appears
to be more severe in patients with hip fracture
than in the general aging population. A low pro-
tein intake could be particularly detrimental for
the conservation of bone integrity with aging
8,9
.
Protein undernutrition can favor the occurrence
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INFLUENCE OF LIFE-STYLE ON OSTEOPOROSIS
of hip fracture by increasing the propensity to fall
as a result of muscle weakness and impairment in
movement coordination; by affecting protective
mechanisms, such as reaction time and muscle
strength, and thus reducing the energy required
to fracture an osteoporotic proximal femur;
and/or by decreasing bone mass (Figure 1)
10
.
Furthermore, a reduction in the protective layer
of soft tissue padding decreases the force required
to fracture an osteoporotic hip.
Protein and osteoporotic fracture
Either a deficient or an excessive protein supply
could negatively affect the balance of calcium
10
.
An indirect argument in favor of a deleterious
effect of high protein intake on bone is that hip
fracture appears to be more frequent in countries
with a high protein intake of animal origin.
However, as expected, countries with the highest
incidence of hip fracture are those with the
longest life expectancy. In a prospective study
carried out in more than 40 000 women in Iowa,
a higher protein intake was associated with a
reduced risk of hip fracture. The association was
particularly evident with protein of animal rather
than vegetal origin
11
. Increasing protein intake
has a favorable effect on bone mineral density
(BMD) in elderly subjects receiving calcium and
vitamin D supplements
12
.
Protein and bone mass
Regarding the relationship to bone mineral mass,
there is a positive correlation with spontaneous
protein intake in premenopausal women
9
. In a
longitudinal follow-up in the frame of the Fram-
ingham Study, the rate of bone mineral loss was
inversely correlated to dietary protein intake
13
.
Taken together, these results indicate that a suf-
ficient protein intake is mandatory for bone
health, particularly in the elderly. Thus, whereas
a gradual decline in calorie intake with age can
be considered an adequate adjustment to the
progressive reduction in energy expenditure, the
parallel reduction in protein intake may be detri-
mental for maintaining the integrity and func-
tion of several organs or systems, including skele-
tal muscles and bone.
Protein replenishment and osteoporosis
A state of undernutrition on admission, which is
consistently documented in elderly patients with
hip fracture, followed by inadequate food intake
Low protein intake
IGF-1
Bone mass
Muscle mass
Fracture risk
Risk of falling
Medical complications
Figure 1 Protein undernutrition in the elderly. Possible role of insulin-like growth factor-I (IGF-I) in bone
mass, muscle mass, risk of fracture and outcome after hip fracture
73
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