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POSTMENOPAUSAL OSTEOPOROSIS
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35. von Wowern N, Klausen B, Olgaard K. Steroid-
induced mandibular bone loss in relation to mar-
ginal periodontal changes. J Clin Periodontol 1992;
19: 182–6
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porosis: a risk factor in periodontal disease. J Peri-
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37. von Wowern N, Klausen B, Hylander E. Bone
loss and oral state in patients on home parenteral
nutrition. J Parenteral Enteral Nutr 1996; 20:
105–9
38. Hildebolt CF, Pilgram TK, Dotson M, et al.
Attachment loss with postmenopausal age and
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39. Mohammad AR, Brunsvold M, Bauer R. The
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40. Mohammad AR, Bauer RL, Yeh C-K. Spinal
bone density and tooth loss in a cohort of post-
menopausal women. Int J Prosthodont 1997; 10:
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association between osteopenia and periodontal
attachment loss in older women. J Periodontol
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42 Payne JB, Reinhardt RA, Nummikoski PV, et al.
The association of cigarette smoking with alveo-
lar bone loss in postmenopausal females. J Clin
Periodontol 2000; 27: 658–64
43. Tezal M, Wactawski-Wende J, Grossi SG, et al.
The relationship between bone mineral density
and periodontitis in postmenopausal women. J
Periodontol 2000; 71: 1492–8
44. Ronderos M, Jacobs DR, Himes JH, Pihlstrom
BL. Associations of periodontal disease with
femoral bone mineral density and estrogen
replacement therapy: cross-sectional evaluation
of US adults from NHANES III. J Clin Periodon-
tol 2000; 27: 778–86
45. Inagaki K, Kurosu Y, Kamiya T, et al. Low
metacarpal bone density, tooth loss, and peri-
odontal disease in Japanese women. J Dent Res
2001; 80: 1818–22
46. Pilgram TK, Hildebolt CF, Dotson M, et al.
Relationships between clinical attachment level
and spine and hip bone mineral density: data
from healthy postmenopausal women. J Periodon-
tol 2002; 73: 298–301
47. Yoshihara A, Seida Y, Hanada N, Miyazaki H. A
longitudinal study of the relationship between
periodontal disease and bone mineral density in
community-dwelling older adults. J Clin Periodon-
tol 2004; 31: 680–4
KD. Longitudinal alveolar bone loss in post-
menopausal osteoporotic/osteopenic women.
Osteoporos Int 1999; 10: 34–40
49. Mohammad AR, Hooper DA, Vermilyea SG, et
al. An investigation of the relationship between
systemic bone density and clinical periodontal
status in post-menopausal Asian-American
women. Int Dent J 2003; 53: 121–5
50. Humphries S, Devlin H, Worthington H. A radi-
ographic investigation into bone resorption of
mandibular alveolar bone in elderly edentulous
adults. J Dent 1989; 17: 94–6
51. Ortman LF, Hausmann E, Dunford RG. Skeletal
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Osteoporosis and reduction of residual ridge in
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49–56
53. Wactawski-Wende J, Grossi S, Trevisan M, et al.
The role of osteopenia in oral bone loss and peri-
odontal disease. J Periodontol 1996; 67: 1076–84
54. Wactawski-Wende J, Hausmann E, Hovey KM,
et al. The association between osteoporosis and
oral bone loss in postmenopausal women. J Peri-
odontol 2005; in press
55 Daniell HW. Postmenopausal tooth loss. Contribu-
tions to edentulism by osteoporosis and cigarette
smoking. Arch Intern Med 1983; 143: 1678–82
56. Aström J, Bäckström C, Thidevall G. Tooth loss
and hip fractures in the elderly. J Bone Joint Surg
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57. Krall EA, Dawson-Hughes B, Papas A, Garcia
RI. Tooth loss and skeletal bone density in
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POSTMENOPAUSAL OSTEOPOROSIS AND DENTAL HEALTH
58. Taguchi A, Tanimoto K, Suei Y, Wada T. Tooth
loss and mandibular osteopenia. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 1995; 79:
127–32
59. Taguchi A, Tanimoto K, Suei Y, et al. Oral signs
as indicators of possible osteoporosis in older
women. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 1995; 80: 612–16
60. Krall EA, Garcia RI, Dawson-Hughes B.
Increased risk of tooth loss is related to bone loss
at the whole body, hip, and spine. Calcif Tissue Int
1996; 59: 433–7
61. Krall EA, Dawson-Hughes B, Garvey AJ, Garcia
RI. Smoking, smoking cessation, and tooth loss. J
Dent Res 1997; 76: 1653–9
62. Bando K, Nitta H, Matsubara M, et al. Bone
mineral density in periodontally healthy and
edentulous postmenopausal women. Ann Peri-
odontol 1998; 3: 322–6
63. Taguchi A, Suei Y, Ohtsuka M, et al. Relationship
between bone mineral density and tooth loss in
elderly Japanese women. Dentomaxillofac Radiol
1999; 28: 219–23
64. Xie Q, Ainamo A. Association of edentulousness
with systemic factors in elderly people living at
home. Community Dent Oral Epidemiol 1999; 27:
202–9
65. May H, Reader R, Murphy S, Khaw K-T. Self-
reported tooth loss and bone mineral density in
older men and women. Age Ageing 1995; 24:
217–21
66. Klemetti E, Vainio P. Effect of bone mineral den-
sity in skeleton and mandible on extraction of
teeth and clinical alveolar height. J Prosthet Dent
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67. Klemetti E, Vainio P, Lassila V. Mineral density in
the mandibles of partially and totally edentate
postmenopausal women. Scand J Dent Res 1994;
102: 64–7
68. Earnshaw SA, Keating N, Hosking DJ, et al. for
the EPIC Study Group. Tooth counts do not pre-
dict bone mineral density in early post-
menopausal Caucasian women. Int J Epidemiol
1998; 27: 479–83
69. von Wowern N. Bone mineral content of
mandibles: normal reference values – rate of age
related bone loss. Calcif Tissue Int 1988; 43: 193–8
70. von Wowern N, Hjorting-Hansen E. The
mandibular bone mineral content in relation to
vestibulolingual sulcoplasty. A 2-year follow-up.
J Prosthet Dent 1991; 65: 804–8
71. Kribbs PJ, Smith DE, Chesnut CH. Oral findings
in osteoporosis. Part II: Relationship between
residual ridge and alveolar bone resorption in
generalized skeletal osteopenia. J Prosthet Dent
1983; 50: 719–24
72. Henrikson P-A, Wallenius K. The mandible and
osteoporosis (1). A qualitative comparison
between the mandible and the radius. J Oral
Rehab 1974; 1: 67–74
73. Solar P, Ulm CW, Thornton B, Matejka M. Sex-
related differences in the bone density of atrophic
mandibles. J Prosthet Dent 1994; 71: 345–9
74. Klemetti E, Collin H-L, Forss H, et al. Mineral
status of the skeleton and advanced periodontal
disease. J Clin Periodontol 1994; 21: 184–8
75. Jacobs R, Ghyselen J, Koninckx P, van Steen-
berghe D. Long-term bone mass evaluation of
mandible and lumbar spine in a group of women
receiving hormone replacement therapy. Eur J
Oral Sci 1996; 104: 10–16
76. Mohajery M, Brooks SL. Oral radiographs in the
detection of early signs of osteoporosis. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 1992; 73:
112–17
77. Payne JB, Zachs NR, Reinhardt, RA et al. The
association between estrogen status and alveolar
bone density changes in postmenopausal women
with a history of periodontitis. J Periodontol 1997;
68: 24–31
78. Civitelli R, Pilgram TK, Dotson M, et al. Alveo-
lar and postcranial bone density in post-
menopausal women receiving hormone/estrogen
replacement therapy: a randomized, double-
blind, placebo-controlled trial. Arch Intern Med
2002; 162: 1409–15
79. Drozdzowska B, Pluskiewicz W. Longitudinal
changes in mandibular bone mineral density
compared with hip bone mineral density and
quantitative ultrasound at calcaneus and hand
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80. Kribbs PJ, Chesnut CH. Osteoporosis and dental
osteopenia in the elderly. Gerodontology 1984; 3:
101–6
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THE CONCEPT OF BONE QUALITY
Osteoporosis has been characterized as a disease
of decreased bone mass. Bones were considered
Accordingly, osteoporosis has been diagnosed
based on a surrogate for bone mass, the areal
bone mineral density (BMD). Treatments have
been developed to prevent bone loss or restore
bone lost, and their efficacy measured by how
well these outcomes are achieved. However, sev-
eral observations from large clinical trials have
exposed the limitations of BMD measurement.
Many fractures occur among patients with nor-
mal BMD
1
, small changes in BMD result in
greater than expected reductions in fracture
risk
2
, reductions in fracture risk are evident
before maximal changes in BMD are achieved
3
and changes in BMD following antiresorptive
treatment explain only a small proportion of the
variance in fracture risk reduction
4
. The term
bone quality has been used to explain these and
other clinical findings that cannot be explained
by BMD measurements. During the past decade,
interest in bone quality has increased dramati-
cally, but the use of the term has been inconsis-
tent, mainly due to the lack of a consensus on an
operational definition.
Four years ago, the term bone quality was
introduced in an updated definition of osteo-
porosis proposed by a National Institutes of
Health (NIH)-sponsored Consensus Conference
on Osteoporosis as ‘a skeletal disorder character-
ized by compromised bone strength predisposing to
an increased risk of fractures’. This statement
asserted that bone strength reflects the integra-
tion of bone quality and bone density
5
. However,
a definition of bone quality and/or bone strength
was not provided. An operational definition of
bone quality has been proposed as the ‘totality of
features and characteristics that influence a
bone’s ability to resist fractures’
6
. What are those
features and characteristics of bone that influence
resistance to fractures?
As structural engineers have long recognized,
the strength of a structure is a function of:
(1) The mechanical properties of the material;
(2) The three-dimensional arrangement of that
material in space;
(3) The amount of material.
The same is true for bone. If we accept that, in
this context, bone strength is the ability to resist
stress and strain, avoiding fracture, bone
strength is a function of material properties, such
as the degree of mineralization, the organic
matrix and the accumulation of microdamage;
structural properties, including geometry and
microarchitecture; as well as the amount of mass.
Bone remodeling optimizes bone mass and dis-
tribution in response to mechanical demand, and
also repairs damaged bone.
The impact of bone remodeling and
age on bone quality
After the menopause, there is an increase in the
rate of bone turnover. It happens immediately
after the menopause and is sustained over time.
Recently, Recker and colleagues
7
measured bone
remodeling rates in transilial biopsy specimens
from 50 premenopausal women before and 1
year after the menopause, and 34 women who
were 13 years past the menopause. Activation
frequency was nearly doubled 1 year after the
menopause, and was tripled 13 years after the
menopause. This rise in the rate of bone remod-
eling has for a long time been considered to be
Bone quality
C. E. Bogado
11
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POSTMENOPAUSAL OSTEOPOROSIS
responsible for the loss of bone mass and the
subsequent increase in the risk of fracture in
postmenopausal osteoporosis. However, bone
remodeling is now widely recognized to be a
fragility factor by itself, independent of BMD. In
a reanalysis of data from clinical trials with estro-
gen therapy in postmenopausal osteoporotic
women, Riggs and colleagues
8
showed that ver-
tebral fracture risk was directly related to the
rate of bone turnover, and increased about four-
fold between low and high levels of turnover,
even in the presence of normal BMD.
Age also contributes to fracture risk. Hui and
associates
9
studied the relationship of fracture
risk to both bone mass and subject age. While
this article confirmed the inverse relationship
between BMD and fracture risk, it showed that
the risk for fracture increases with age at any
level of bone mass. Older subjects had several-
fold the fracture risk of young subjects at the
same bone mass.
Age and bone remodeling imbalance impact
on both the material and structural determinants
of bone strength.
The structural properties of bone
In order to avoid fracture, bone needs to be both
stiff and tough. In part, this is achieved by struc-
tural adaptation. Long bones are fashioned as a
cortex of highly mineralized tissue placed distant
from the central long axis, a design that confers
maximum resistance to bending (stiffness). In
contrast, vertebral bodies consist of a mineral-
ized interconnecting honeycomb of plates, a
structure that can absorb energy by deformation
(toughness).
Aging is accompanied by changes in trabecu-
lar bone microarchitecture that affect bone
strength. There is progressive trabecular thin-
ning, conversion from a plate-like to a rod-like
structure and loss of connectivity, with preferen-
tial loss of horizontal trabeculae
10
. The loss of
horizontal trabeculae results in a dramatic reduc-
tion in compressive strength
11
. According to
Euler’s theorem, the strength of a vertical tra-
becula is inversely proportional to the square
power of its effective length
12
. Therefore, the loss
of a horizontal strut or cross-tie increases the
effective length of a vertical trabecula by a factor
of two, but will reduce its compressive strength
by a factor of four.
The remodeling process is also a source of
structural weakness. The resorption cavities act
as stress raisers by concentration of the mechan-
ical stress imposed on bones. A high turnover
rate produces an increase in the number and
depth of resorption cavities, resulting in micro-
damage accumulation, trabecular perforation
and loss of connectivity.
Cortical bone also deteriorates with age. Long
bones suffer a continuous process of bone resorp-
tion at the endosteal surface that is compensated
by periosteal apposition, resulting in bone expan-
sion with age. In women, after the menopause,
there is an increase in endocortical remodeling.
Since periosteal apposition is insufficient to com-
pensate for the bone loss at the endosteal surface,
there is a progressive thinning of the cortex. The
increase in cross-sectional area maintains the
bending stress until a point where the structure
becomes unstable and susceptible to fracture.
Furthermore, there is an increase in cortical
porosity with age, which is more evident in
women, and contributes to bone fragility
13
.
The material properties of bone
The required levels of toughness and stiffness can
also be achieved by adaptation of the relative
amounts of the organic and mineral constituents
of bone. The degree of mineralization is one of
the most, if not the most, important material
property of bone.
After bone resorption, bone formation is a
multistep process. At each bone remodeling unit,
after the organic matrix is deposited, there is a
fast process of primary mineral apposition that
yields a low-mineralized bone. This is followed
by a slow and gradual secondary mineralization,
including an increase in crystal number and crys-
tal size. The duration of this process depends on
the level of bone remodeling. Therefore, an
imbalance in the rate of bone remodeling affects
the bone tissue mineral content. If the remodel-
ing rate is high, older, more mineralized bone is
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BONE QUALITY
replaced by younger, less mineralized bone. In
contrast, if remodeling decreases, more time is
available for secondary mineralization. The
degree of mineralization of bone shows a high
correlation with bone strength when it is meas-
ured by compressive testing of bone biopsy sam-
ples
14
. However, there is a complex relationship
between mineralization and bone strength. The
greater is the tissue mineral content, the greater
are the stiffness and the peak stress that the bone
will tolerate. However, increasing mineral con-
tent is associated with declining toughness.
Highly mineralized bone becomes brittle and
will not be able to absorb energy without crack-
ing upon impact loading. Animal studies have
suggested that high mineralization following
pharmaceutical suppression of remodeling is
associated with microdamage accumulation
15
.
Microdamage accumulation significantly reduces
toughness and may decrease fracture resist-
ance
16
. Moreover, it has been suggested that
microfractures need less energy to propagate in
homogeneous composite materials, as is the case
in older, highly mineralized bone
17
. However,
the extent of damage accumulation necessary to
increase fracture risk significantly is unclear, and
it has been suggested that, while the accumula-
tion of microdamage is associated with reduced
toughness, the ability of a material to undergo
microcracking may increase its toughness. The
role of damage accumulation in fracture risk
remains unclear.
CAN BONE QUALITY BE
MEASURED?
At present, there are no suitable techniques for
the measurement of material properties of bone
in the clinical setting. Similarly, the assessment of
trabecular microarchitecture has been restricted
to invasive techniques such as histomorphometry
or micro-computed tomography (CT) of bone
biopsy samples, because most available non-
invasive imaging techniques lack the resolution
required for such purposes. However, a new
generation of high-resolution peripheral quanti-
tative CT scanners with acceptable levels of radi-
ation dose for clinical use have recently become
available. It allows the measurement of both
densitometric and architectural parameters for
cortical and trabecular bone separately. Even
more important, three-dimensional (3-D) images
can be obtained, opening the door to in vivo
assessment of bone mechanical competence in
the near future
18
.
Another recent development is the combina-
tion of a specifically designed magnetic reso-
nance (MR) detection coil and image processing
software that provides a highly detailed 3-D
model of bone architecture using a standard clin-
ical magnetic resonance imaging (MRI) scanner.
In addition to standard structural histomor-
phometry, topology parameters, such as plate-
to-rod ratio, can be obtained. Structural parame-
ters could be more sensitive to individual
differences than bone density. A study using this
micro-MRI technique showed that two groups of
postmenopausal women – with and without ver-
tebral fractures – with similar BMD values at
both hip and lumbar spine could be discrimi-
nated based on the deterioration of topology
parameters
19
.
There is also some progress in the assessment
of cortical bone geometry. It is mentioned above
that at some point the aging cortical cortex can
become unstable and susceptible to fracture.
Engineers estimate the stability of thin-walled
tubes under bending stress by calculation of the
buckling ratio. The buckling ratio has been cal-
culated from estimated geometric parameters
obtained from standard dual-energy X-ray
absorptiometry (DXA) scans of the hip, a tech-
nique known as hip structure analysis
20
. It has
been suggested that estimation of the buckling
ratio can predict the risk of fracture. Crans and
colleagues
21
calculated the baseline buckling
ratio in patients from the placebo arm of the
Multiple Outcomes of Raloxifene Evaluation
(MORE) study, using hip structure analysis.
There was a significant relationship between
baseline femoral neck buckling ratio and 3-year
vertebral fracture risk, and a significant relation-
ship between the baseline intertrochanter buck-
ling ratio and vertebral, non-vertebral and hip
fracture risk at 3 years. The estimation of buck-
ling ratio could also be a sensitive tool for the
assessment of treatment efficacy. A study in a
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POSTMENOPAUSAL OSTEOPOROSIS
subset of patients from a large clinical trial on the
effects of daily injections of PTH (1–34) (teri-
paratide) in postmenopausal osteoporotic women
showed a decrease in femoral neck buckling ratio
after 18 months of treatment
22
. Hip structure
analysis has severe limitations, and these results
should be considered as preliminary. However,
the buckling ratio could be calculated from
imaging techniques other than DXA that allow
more precise measurements of geometric proper-
ties of bone, such as quantitative computed
tomography (QCT) or peripheral QCT (pQCT).
CONCLUSIONS
There are opportunities for improvement in the
identification of those at greatest risk for frac-
ture, and monitoring the response to treatment.
New techniques for non-invasive measure-
ment of structural determinants of bone strength
could very soon find their way from research to
the clinic.
In contrast, the non-invasive measurement of
bone material properties remains elusive, and
worthy of additional research effort.
100
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BONE QUALITY
increases microdamage accumulation and reduces
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ence of microdamage on fracture toughness of the
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composites. Proc R Soc London 1975; 341: 409–28
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(Suppl 5): S89–99
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tal topological analysis of in-vivo magnetic reso-
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femoral neck strength from bone mineral data. A
structural approach. Invest Radiol 1990; 25: 6–18
21. Crans GG, Beck TJ, Semanik LM, et al. Baseline
buckling ratio derived from hip structure analysis
predicts the risk of nonvertebral fractures. J Bone
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Diagnosis: clinical, hormonal and biochemical
evaluation
D. M. Reid
12
INTRODUCTION
This paper examines the value of clinical risk fac-
tors for osteoporosis and their role in identifying,
first, risk factors that are associated with fracture
and, second, risk factors associated with low bone
density that can be used to stimulate a measure-
ment of bone mass to enable a clinical diagnosis.
Hormonal assessments are generally required to
identify secondary osteoporosis and the causes of
secondary osteoporosis. The tests frequently car-
ried out to exclude these disorders are described.
Finally, the role of biochemical measurements of
bone turnover for predicting fracture, identifying
secondary osteoporosis, targeting successful
treatment and monitoring treatment efficacy are
discussed.
A good starting point is to examine the defi-
nition of osteoporosis as discussed in the
National Institutes of Health Consensus 2001
1
.
The consensus statement defines osteoporosis as
‘a skeletal disorder characterized by reduced
bone strength predisposing a person to an
increased risk of fracture’. The consensus state-
ment progresses to describe bone strength as pri-
marily reflecting an integration of bone density
and bone quality.
The consensus statement further defines the
main predictors of low bone density in an indi-
vidual as low body mass index, a family history of
osteoporosis, smoking and prior fracture, late
menarche, early menopause and low estrogen
levels. Predictors of high bone density include
grip strength and current exercise. The role of
predictors of falls is not ignored and these
include slow gait speed, decreased quadriceps
strength, impaired cognition, impaired vision
and presence of environmental hazards. There
are also identified predictors of fracture occurring
after a fall, and these include those of a tall dis-
position, those individuals who fall to the side
and bone geometry, for example femoral neck
length or shape.
PREDICTORS OF FRACTURES
It is useful to review which factors are associated
with site-specific osteoporotic fractures and those
that are associated with all fractures of bone sites
considered to relate to osteoporosis. Multiple risk
factors for fracture have been described as shown
in Table 1. While low bone mineral density
(BMD) is a major risk factor, it is important to
realize that some known factors are independent,
or partly independent, of BMD
2
. Prominent
among these are age and previous fragility frac-
ture, which may in part be due to the influence
of falls, which increase in incidence with age and
pre-date most, but not all, fractures.
Some of the relationship to fall risk and an
interaction with low BMD can be seen in a
recent analysis that has been published from the
OFELY (Os des Femmes de Lyon) study, of a 5-
year follow-up of 672 women who suffered 81
fractures (24 vertebral, 16 risk, nine hip, five
humerus, 11 ankle, etc.)
3
. Significant predictors
of fracture from the study are shown in Table 2.
It will be seen that the most prominent factors
amongst those identified are previous fracture,
low total hip bone density, low physical activity
score, low grip strength and increasing age,
which, in this particular study, applied to those
over the age of 65. A further paper has very
recently been published from the United King-
dom examining a shorter follow-up of a larger
103
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