Introduction and objectives: coeliac disease (CD) affects
around 1-2 % of the world population. Most patients are now diag-
nosed when adults, suffering the consequences of an impaired bone
mineralization. This review aims to provide an updated discussion
on the relationship between low bone mineral density (BMD),
osteopenia and osteoporosis, and CD.
Methods: a PubMed search restricted to the last 15 years was
conducted. Sources cited in the results were also reviewed to identify
potential sources of information.
Results: low BMD affects up to 75 % of celiac patients, and
can be found at any age, independently of positive serological mark-
ers and presence of digestive symptoms. The prevalence of CD
among osteoporotic patients is also significantly increased. Two the-
ories try to explain this origin of low BMD: Micronutrients malab-
sorption (including calcium and vitamin D) determined by villous
atrophy has been related to secondary hyperparathyroidism and
incapacity to achieve the potential bone mass peak; chronic inflam-
mation was also related with RANKL secretion, osteoclasts activation
and increased bone resorption. As a consequence, celiac patients
have a risk for bone fractures that exceed 40 % that of matched
non-affected population. Treatment of low BMD in CD comprises
gluten-free diet, calcium and vitamin D supplementation, and biphos-
phonates, although its effects on CD have not been specifically
Conclusions: up to 75 % of celiac patients and 40 % of that
diagnosed in adulthood present a low BMD and a variable increase
in the risk of bone fractures. Epidemiological changes in CD make
bone density scans more relevant for adult coeliacs.
Key words: Coeliac disease. Osteoporosis. Osteopenia. Bone min-
eral density. Densitometry.
A low bone mineral density (BMD) constitutes the first
diagnostic criterion for osteoporosis, a skeletal metabolic
disease further defined by impaired bone microarchitecture,
increased bone fragility and susceptibility to bone fractures.
The availability of bone density scan as a non-invasive
diagnostic technique uncovered the link between this bone
disorder and coeliac disease (CD) relatively few years ago
(1,2). By contrast, the association between child osteoma-
lacia and CD has been known since the first descriptions
of the latter disease, even before the origin and treatment
of CD itself were known (3). Osteomalacia is a disease
characterized by low BMD, marked bone deformities and
rickets, which, on rare occasions, is part of the initial pre-
sentation of CD (4,5).
CD is a highly prevalent disease (6) that affects around
1 % of the world population according to serology-based
screening studies (7). While CD has been traditionally
considered a childhood-onset disorders predominantly, it
is now conclusively demonstrated that most patients are
diagnosed when adults, as also corroborated in our country
(8,9), among whom both atypical manifestations and a
low suspicion index may delay the diagnosis (10). In fact,
most CD sufferers are undiagnosed, and women are more
frequently diagnosed than men. Many current CD patients
lived with their symptoms for years before diagnosis, and
were therefore exposed to the consequences of the disease.
Furthermore, osteoporosis presents characteristics similar
to those of CD in terms of frequency and underdiagnosis.
It has been hypothesized that CD could explain part of
the considerable “mixed bag” represented by idiopathic
Bone mineral density in adult coeliac disease: An updated review
Alfredo J. Lucendo1and Alvaro García-Manzanares2
Departments of 1Gastroenterology and 2Endocrinology and Nutrition. Hospital General de Tomelloso. Tomelloso,
Ciudad Real. Spain
REVISTA ESPAÑOLA DE ENFERMEDADES DIGESTIVAS
Copyright © 2013 ARÁN EDICIONES, S. L.
REV ESP ENFERM DIG (Madrid)
Vol. 105. N.° 3, pp. 154-162, 2013
Correspondence: Alfredo J. Lucendo. Department of Gastroenterology. Hos-
pital General de Tomelloso. Vereda de Socuéllamos, s/n. 13700 Tomelloso,
Ciudad Real. Spain
POINT OF VIEW
Lucendo AJ, García-Manzanares A. Bone mineral density in adult
coeliac disease: An updated review. Rev Esp Enferm Dig 2013;
Vol. 105. N.° 3, 2013 BONE MINERAL DENSITY IN ADULT COELIAC DISEASE: AN UPDATED REVIEW 155
REV ESP ENFERM DIG 2013; 105 (3): 154-162
osteoporosis (1,11-13) Therefore, a high rate of suspicion
among health professionals treating both diseases (CD
and osteoporosis) and using their best knowledge could
bring many hidden cases to light, with the benefit of accu-
rate and early treatment.
In adult patients, changes in bone mineralization,
osteopenia or osteoporosis represent one of the most com-
mon complications of CD, and can affect up to 75 % of
patients in some series (1) with a prevalence among coeliac
sufferers that is double that of the unaffected population in
the same age range (11). Despite this, and the many studies
on the subject notwithstanding, a description of how CD -
a primarily digestive disorder- can affect bone metabolism
has yet to be fully elucidated.
CD in itself causes significant deterioration in quality
of life (14-16), which is compounded by the presence of
osteoporosis and its clinical manifestation as fractures.
These and other factors are reasons for physicians to adopt
an interventionist stance and try to prevent its occurrence
and/or mitigate its impact.
OSTEOPOROSIS: DEFINITION AND GENERAL
Osteoporosis is the most common metabolic bone dis-
ease. It involves a reduction in bone mass and is responsible
for most fractures suffered by adults over 50. It is estimated
that 1 in 3 women over 50 in Europe (17) and the United
States (18) will suffer an osteoporotic fracture during their
lifetimes. Although BMD is considered the major determi-
nant of osteoporosis, there are additional factors that influ-
ence bone fragility, which, in recent years, have been
brought together under the term “bone quality.” These
include microarchitecture, the degree of bone turnover, the
build-up of lesions or microfractures and the degree of bone
The World Health Organization establishes different
degrees of low bone mass based on bone density scan mea-
surements of any skeletal area in American Caucasian
women (20). This strategy establishes a diagnosis of osteo-
porosis when bone mass values are below -2.5 standard
deviations (SD) of peak bone mass (i.e. the maximum
BMD value reached by an adult), and osteopenia when
those values are located between -1 SD and -2.5 SD.
Severe or established osteoporosis is that presenting with
a BMD less than -2.5 SD and a current or past fragility
fracture (18,21). The results of BMD measurements are
expressed as a T-score, which is the number of standard
deviations by which BMD measurement differs from bone
density measurement in the young population (“peak”
BMD) (Table I). Another way of expressing the results is
the Z-score, which is obtained by comparing a BMD mea-
surement with reference values for subjects of the same
age and gender. It is recommended in some guidelines (22)
for men and for premenopausal women.
PREVALENCE OF OSTEOPOROSIS AMONG
COELIAC DISEASE PATIENTS
It is estimated that by the time childhood CD is diag-
nosed, one-third of affected children have osteoporosis,
one-third have osteopenia and only the remaining third
retain a normal BMD (12). In any case, once the gluten-
free diet (GFD) is instituted, most coeliac children catch
up to their height-weight growth curve and accelerate their
rate of bone mineralization, so that most achieve normal
peak bone mass by the time bone growth is completed. The
main problem arises when CD is diagnosed during adult-
hood, once bone growth is complete and peak bone mass
has been reached. Among these patients, the prevalence of
osteoporosis is at least twice that of the unaffected popu-
lation in the same age range (11,23). More than half of
asymptomatic coeliac patients with positive serological and
digestive tract markers may have bone disease at the time
of diagnosis (1,13,24-28). This even includes those without
villous atrophy, that is, at stages 1 and 2 of the Marsh-Ober-
huber classification for duodenal lesion.
Prevalence studies of bone mass loss among patients
with CD reveal widely variable frequencies (2,24,29-36)
(Table II); Valdimarsson et al. carried out a prospec -
tive study of 63 adult patients and noted a prevalence of
Table I. World Health Organization (WHO) diagnostic
criteria for post-menopausal Caucasian women
Diagnosis BMD criteria (T-score)
Normal BMD T > - 1 SD
Osteopenia or low bone density BMD T < - 1 and > -2.5 SD
Osteoporosis BMD T < - 2.5 SD
Severe osteoporosis BMD T > - 2.5 SD + fracture
T-score: Comparison with BMD value in average reference population; SD: Standard
deviation; BMD: Bone mineral density.
Table II. Studies of BMD in adult patients with coeliac
disease before starting GFD (adapted from Scott, 2000) (31)
Parameter Mean weighted Number of studies
value (number of
Z-score, lumbar spine -1.3 14 (490)
Z-score, hip -1.1 7 (239)
T-score, lumbar spine -1.7 1 (86)
T-score, hip -1.4 1 (86)
% with lumbar osteoporosis 26 6 (212)
% with hip osteoporosis 11 3 (102)
% with lumbar osteopenia 41 4 (188)
% with hip osteopenia 43 3 (102)
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REV ESP ENFERM DIG 2013; 105 (3): 154-162
osteoporosis of 22 % in the forearm, 18 % in the hip and
15 % in the lumbar spine (estimated on the basis of Z-
scores) (37). Bardella et al. only documented low BMD
among women diagnosed with CD during adulthood (38).
Meyer et al. found low BMD in the lumbar spine in 38 %
and in the hip in 44 % of the adult coeliac patients analysed
(36). The wide variability in the frequency of low BMD in
these studies may be explained by several factors, including
the diagnostic criteria for osteoporosis (T or Z-score), the
measurement method, the skeletal location where the mea-
surement was obtained, patient selection, and whether
assessment was performed before or after a GFD was start-
ed. In any case, the available data confirm a clearly height-
ened prevalence of low BMD among coeliac patients com-
pared to the general population, which generally ranges
around 40 %.
Low BMD has been demonstrated in patients with classic
symptoms (14), in sub-clinical cases (39), and even in
asymptomatic patients (29). Paradoxically, even greater
impairment has been observed among patients without
digestive symptoms than among those with classic symp-
toms (13). Therefore, the type of CD-related symptom does
not seem to predict the presence of low BMD, which
explains attempts to identify other determinants.
Osteoporosis is therefore a common complication of
CD, which suggests that it is appropriate to consider
whether or not to screen for CD in patients with idiopathic
osteoporosis. Although there is no definitive consensus,
the greater weight of opinion is in favour of this strategy
(40-43), as the frequency of CD is 10 times higher than
expected in patients with osteoporosis; in fact, a similar
frequency of CD among type 1 diabetics already justifies
universal screening among these patients (44). Moreover,
CD screening through specific antibodies in patients with
OS has led to diagnosis of between 4 (45) and 17 (43) times
Results from studies where results were opposed to
screen CD patients for osteoporosis can be explained due
to the use of low-sensitivity antibodies; in fact, Legroux-
Gerot et al. only measured anti-gliadin antibodies, while
tissue anti-transglutaminase (AAtTG) was only determined
in those with positive titres (46), a strategy that underdiag-
noses CD. This same study established the AAtTG posi-
tivity threshold at 50 U/ml, well above the 2 U/ml threshold
currently recommended for diagnosing adults (47). Other
studies suffer from similar limitations: Mather et al. mea-
sured antiendomysial antibodies (48), Lindh et al.
antigliadin (45), and the positivity threshold for AAtTG in
Laadhar’s research was set at 10 U/ml (42).
AETIOLOGY AND PATHOGENESIS
OF LOW BMD IN CD
The pathogenic mechanisms underlying metabolic bone
disease in patients with CD have not been fully elucidated.
The origin of osteoporosis in CD has been classically
associated with malabsorption caused by intestinal villous
atrophy and poor absorption of calcium and vitamin D
(49), as well as secondary hyperparathyroidism (50). Low
consumption of dairy products (51), failure to ever reach
peak theoretical bone mass (29,52-54), higher degree of
duodenal injury in biopsies (55), and greater delay in diag-
nosis (23) have also been directly related to the pathogen-
esis of low BMD in coeliac patients.
We know that vitamin D deficiency is common among
patients with CD, although there are no changes in the
expression of vitamin D receptors (56) or a greater number
of receptor gene mutations interfering with the metabolism
of this vitamin (57) in this population. Restricted milk intake
may exacerbate vitamin D deficiency; in fact, co-occurrence
of lactose intolerance is common among coeliac patients,
and is estimated at 10 %, but may increase to 50 % in pres-
ence of obvious symptoms of malabsorption (58-61). How-
ever, one must bear in mind that diet only provides 5-10 %
of required vitamin D (62), with the rest being obtained
from exposure to sunlight. Even so, studies of coeliac
patients have failed to establish any clear association
between vitamin D levels and bone impairment. This is also
the case for other intestinal diseases, such as inflammatory
bowel disease (62).
Several authors have suggested that deficits in other fat-
soluble vitamins (A, K and E) and even water-soluble vit-
amins (C, B12, folic acid and B6) or minerals (such as iron,
calcium, phosphorus, copper, zinc, boron, fluorine), which
are all required for normal bone metabolism (55,63), also
result from the intestinal malabsorption exhibited by coeliac
Hyperparathyroidism is another implicated factor; even
in patients with normal vitamin D serum levels, high PTH
levels have been associated with bone mass loss (50).
Indeed, coeliac patients on a GFD frequently exhibit high
serum PTH levels (64). Reduced serum levels of IGF-1
(insulin-like growth factor-1 or somatomedin C) (65) con-
stitutes an additional hormonal factor which has been
involved in patients with a lower bone mass. This was asso-
ciated with decreased serum levels of zinc (66), which nor-
malized after introduction a GFD.
Despite the above, the malabsorption theory in and of
itself has not been corroborated in some studies (55), while
the complex regulation of bone turnover and the effect
of the multiple nutritional factors involved, together with
the discordant results of various studies, have led to the
emergence of new hypotheses for the origin of osteoporosis
in CD, such as the link between low BMD and chronic
inflammation (67). Indeed, a less well-known function of
vitamin D is its role in the activation of T lymphocytes that
maintain the integrity of intestinal mucosal immunity, pre-
vent infection (68) and regulate protein binding (69).
Accordingly, vitamin D deficiency has long been considered
a trigger of autoimmune and inflammatory diseases (70).
Chronic inflammation determines changes in bone
metabolism via several proinflammatory cytokines, such
as tumour necrosis factor alpha (TNF-α), interleukins
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(IL)-1beta, IL-6 or gamma interferon. TNF-related
cytokines include the receptor activator of nuclear factor
kappa-B (RANK), its ligand (RANKL), and osteopreote-
gerin (OPG). RANKL is a key molecule in the regulation
of bone metabolism; its genetic expression is induced after
activation of T lymphocytes and it is secreted by these
cells. RANKL has proved to be a survival factor whose
primary function is activation of osteoclasts, cells involved
in bone resorption (71). Overproduction of RANKL is
implicated in a variety of degenerative diseases of bone
tissue, such as rheumatoid arthritis or psoriatic arthritis,
while RANKL gene inactivation in mice produces severe
osteopetrosis caused by a massive osteoclast deficit
(72,73). Conversely, OPG (osteoprotegerin, “for bone pro-
tection”) is an osteoclastogenesis-inhibiting protein, which
acts as a decoy receptor homologous to RANK, binds to
its ligand RANKL, and thereby neutralizes its action (74).
OPG production is stimulated in vivo by oestrogens and
by the anti-resorptive drug strontium ranelate (75). IL-6
promotes the expression of both RANKL and OPG, and
stimulates both osteoblast formation and bone resorption.
Serum levels of RANKL and OPG are high in patients
with CD (76), and the relative relationship established
between these cytokines is therefore more important than
their actual levels; hence, an imbalance in the OPG/RAN-
KL ratio has been associated with altered bone turnover
in patients with different conditions, including renal
osteodystrophy (77), rheumatoid arthritis (78), Cushing’s
disease (79) and primary biliary cirrhosis (80). The
OPG/RANKL ratio is directly associated with IL-6 serum
levels (79) and lumbar bone mass (81). Thus, adult women
with CD have OPG/RANKL ratios significantly lower
than controls despite adherence to a GFD; this correlates
with a lower lumbar BMD (82). Although the role of high
OPG levels in CD has not been fully elucidated, the avail-
able evidence suggests that this is a protective mechanism
against other factors that cause bone damage. The mech-
anisms described as direct activators of osteoclastogenesis
and subsequent bone mass loss (83) have recently been
recognized as potential contributors to osteoporosis among
patients with a range of digestive diseases. In fact, patients
with CD and inflammatory bowel disease have similar
profiles in terms of expression of bone metabolism regu-
latory cytokines (84-86).
Finally, the aetiology of osteoporosis in CD of course
includes factors shared with the rest of the population (87)
(family history, age, menopause, physical activity, smok-
ing), as well as other specific factors such as genetic influ-
ence, the above-mentioned vitamin deficiencies, hormonal
changes and the inflammatory process itself.
Years of exposure to gluten in the diet before diagnosis
do not appear to influence BMD significantly (29,35,
36,88,89) nor does early menopause (27). Some studies
report an inverse relationship between GFD and calcium
intake (90). There is little data on the influence of patient
sex on BMD, but most studies show no difference in this
respect (27,36,37,91,92). Another factor associated with
poor bone condition is a low body mass index (BMI)
(14,55,87,93). Patients with persistent villous atrophy
despite proper adherence to the GFD (refractory CD) are
particularly susceptible to osteoporosis, with a prevalence
of 58 % compared to the 22 % reported among GFD-
responsive patients (93).
DIAGNOSIS OF LOW BONE MINERAL
DENSITY IN CD
All patients in whom there is clinical suspicion of osteo-
porosis should undergo a thorough history-taking and phys-
ical examination so as to identify other risk factors and/or
consequences. As for imaging methods, conventional radi-
ography has not proven to be a specific or sensitive method
for assessment of changes in bone mass; therefore, osteo-
porosis studies should be performed using bone density
scans. In the case of CD, it has been suggested that all
patients diagnosed in adulthood should undergo bone den-
sitometry (14,94), as it is a simple, non-invasive and highly
accurate (95) diagnostic method (the margin of error is esti-
mated at only 5-6 %). Its greatest benefit is determining
whether there is osteoporosis and the degree of impairment,
so that a treatment regimen can be planned. However, some
studies, seeing the low risk of bone fracture among coeliac
patients, have questioned the utility of routine bone density
scan (31,96), as it is considered to have low cost-effective-
ness. Other authors suggest using densitometry only in
patients with digestive conditions (97), even though this is
not a conditioning factor for greater risk (98). In fact, coeliac
patients without gastrointestinal symptoms may have low
BMD, which increases after start of the GFD (13). Recent
studies advocate densitometric assessment in all coeliac
patients diagnosed during adulthood who have villous atro-
phy on duodenal biopsies and/or laboratory values sugges-
tive of malnutrition or malabsorption, regardless of their
Another issue raised in the literature concerns the optimal
timing for bone density scan in coeliac patients -whether
at the time of CD diagnosis or after a period of adherence
to the GFD. In fact, coeliac children show a great bone
recovery capacity after starting a GFD, so no further studies
seem to be necessary until their growth period is completed.
In any case, the main benefit of BMD testing would be
obtained when the introduction of a different treatment
rather than the GFD alone are derived from test results.
As development of osteoporosis is determined by mul-
tiple risk factors, identifying which of these factors are most
relevant, or using a score for the risk of fracture at 10 years,
is highly desirable. Markers of bone remodelling (such as
the N-terminal telopeptide of procollagen-1, hydroxypro-
line, and bone alkaline phosphatase) provide additional
information on the dynamics of bone turnover that is com-
plementary to densitometry findings. In coeliac patients
with osteoporosis, levels of these markers are higher than
in coeliacs with normal BMD (55). However, the usefulness
158 A.J. LUCENDO AND A. GARCÍA-MANZANARES REV ESP ENFERM DIG (Madrid)
REV ESP ENFERM DIG 2013; 105 (3): 154-162
of their determination in the diagnosis of bone diseases is
limited, so measurement is not recommended as part of the
routine evaluation of patients with osteoporosis.
BONE FRACTURE RISK IN CD
Due to the increased prevalence of osteoporosis, coeliac
patients have a high risk of fracture, estimated at between
3.5 to 7 times higher than that of the unaffected population
of the same age and gender (14). Furthermore, up to one
in four adult CD patients have an established history of
fractures (99), which produces significant deterioration in
quality of life.
As in other aspects of the relationship between CD and
osteoporosis, quantification of fracture risk by different
studies shows mixed results. These discrepancies are largely
due to the way in which the data were collected -mainly
from fracture reports, questionnaires, or hospital admis-
sions. It is therefore possible that the prevalence of fractures
(vertebral, hip, and overall) is underestimated in the coeliac
population. One of the common issues of fracture risk stud-
ies is that they lack proper morphometric assessment of the
spine, which underestimates fractures at that level (2), or
failure to use validated questionnaires or methods, such as
the FRAX®(Fracture Risk Assessment Tool) index pro-
posed by the World Health Organization (100).
To date, nine published studies and one meta-analysis
have estimated the incidence or prevalence of bone fractures
in the adult coeliac population (31) (Table III). Their het-
erogeneous methodologies, use of different cut-off points
for determination of osteoporosis, and variable diagnostic
criteria for CD translate into significant discrepancies in
results. A study conducted in Argentina on 165 coeliac
patients retrospectively determined a prevalence of periph-
eral fractures over 3 times higher than that observed in con-
trols (2). The same study showed that the highest prevalence
of fractures in the lumbar spine was only present in patients
with “classic symptoms” of CD (101). A retrospective study
carried out in the UK showed that 21.3 % of coeliac patients
had a history of fractures, compared with only 2.7 % of
non-coeliac controls, a highly significant difference quan-
tified as a relative risk (RR) of 7.0 (102). By contrast, other
studies with large sample sizes in the same geographical
region found no major differences (32). Two further
researches in Europe, the first with a large number of
patients, reported a slight increase in risk of fracture: a study
of approximately 13,000 patients and 65,000 controls in
Sweden showed a 2.1 % higher risk (95 %CI: 1.8-2.4) ofhip
fracture and a 1.4 % higher risk (95 %CI: 1.3-1.5) of any
type of fracture among coeliacs (34). A recent study of adult
coeliacs in Spain, conducted at the time of diagnosis, used
the FRAX®tool to estimate the risk of fracture at 10 years.
This showed a moderate risk of fracture among patients
with duodenal villous atrophy (Marsh stage III), which was
3.5 times that of patients without villous atrophy (Marsh
stage I or II) (55).
Finally, the Olmos et al. meta-analysis (104), which
included 21,000 coeliac patients and about 100,000 con-
trols, confirmed a 43 % increase in the prevalence of frac-
tures among coeliacs (8.7 vs. 6.1 %).
TREATMENT OF LOW BONE MINERAL
DENSITY IN PATIENTS WITH CD
The first-line treatment for osteoporosis in CD is GFD
itself: Many studies have demonstrated its effect on bone
density and calcium absorption (24,26,27,30,35,90-93,105-
108). The greatest bone mass gain described in these studies
is during the first year (27,37): GFD leads to a 5 % increase
in bone mass after 1 year (1), although this is not enough
for bone mass to normalise. In clinical practice conditions,
the degree of adherence to the GFD also determines the
recovery of bone mass, which is generally estimated at
around 30 % (109,110). Furthermore, the recovery rate is
higher in young coeliac patients (24) than among adults
(24,37), which is largely explained by the fact that 97 % of
bone mass is gained in the first two decades of life and full
recovery is difficult after this time.
BMD loss associated with paediatric CD responds to
GFD continuously and gradually, with almost complete
restoration of bone mass after about two years’ treatment
(111). The earlier the age at which the GFD is started, the
better and faster the response (29). In fact, it is estimated
that an increase in BMD will only take place if the GFD is
started before the age of 25 (49). Proper GFD is so impor-
tant for bone metabolism that lack of improvement in BMD
after its introduction has been associated with persistent
duodenal lesions (14).
In addition to the GFD, and in accordance with the NIH
consensus statement on the treatment of osteoporosis (18),
adequate daily intake of calcium and vitamin D should be
ensured, as it is a critical factor for bone mass acquisition
and maintenance. Untreated adult coeliac patients have
shown a 45 % reduction in calcium absorption followed by
an improvement of 52 % after 6 months of GFD adherence
(112). Regarding vitamin D, at the time of diagnosis, less
than 5 % of Spanish adult CD patients had normal serum
levels (55). A daily intake of 1,200-1,500 mg calcium and
800 U vitamin D is recommended, and as in all other forms
of osteoporosis, this should be supplemented with medica-
tions. Adherence to drug therapy, as to the GFD, is a crucial
aspect of treatment, so patients must be kept motivated. In
fact, these patients will most commonly abandon treatment
with calcium and vitamin D, as it must be taken daily, while
hormonal therapy and bisphosphonates (which are admin-
istered weekly) are usually adhered to correctly (113). Drug
treatment would be indicated for patients who do not
achieve bone mass recovery goals, and would not differ
from that established for other causes of osteoporosis, with
bisphosphonates being the recommended first-line therapy.
However, the literature is lacking in data on the specific
effect of bisphosphonates on CD-associated osteoporosis.
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Table III. Available studies on bone fracture risk in adult coeliac disease (adapted from Scott, 2000) (28)
Country and year Study population
Risk of fracture
Vasquez et al. (2)
165 coeliacs and 165
Dual energy X-ray
OR 3.5 (1.8-7.2)
OR 2.8 (0.7-11.5)
Fickling et al. (102)
75 coeliacs with 75 controls
Dual energy X-ray
21 % among coeliacs,
matched by age and sex
absorptiometry (DEXA) of
versus 3 % in controls
lumbar spine and femoral neck
Thomason et al. (32)
244 coeliacs born after 1950, Analysis of coeliac
Lifestyle and general health
OR 1.05 (0.68-1.62)
161 controls of the same
questionnaire, with specific
OR 1.21 (0.66-2.25)
age and sex
Controls paired for
questions about history of
age and sex
West et al. (99)
4732 coeliacs (1589
Codified registry of fractures
HR 1.30 (1.16-1.46)
"incidents") and 23620
study from a database
in coeliacs and controls
HR 1.90 (1.20-3.02)
controls matched by age
HR 1.77 (1.35-2.34)
Moreno et al. (101)
148 coeliacs and 292 controls Cross-sectional study of
History of fracture based on
OR 5.2 (2.8 to 9.8) in
of the same age and sex with cases and controls
interview with a predefined
OR 1.7 (0.7 to 4.4) in
Vestergaard et al. (34)
1021 coeliacs and 3063
Diagnoses of fractures
RRI 0.7 (0.45-1.09)
controls matched by age
of all national hospital
in cases and controls in the
RRI 2.14 (0.70-6.57)
admissions and discharges same national registry
Distal radius (Colles)
RRI 2.00 (0.58-6.91)
Neck of femur
RRI 0.71 (0.27-1.89)
Davie et al. (103)
383 coeliac women over 50
Detailed questionnaire about
OR 1.51 (1.13-1.5)
and 445 controls
history of fractures
Ludvigsson et al. (34)
13000 individuals with CD
Cross-sectional population Records of 1st documented
HR 1.4 (1.3-1.5)
(4819 adults) and 65000
cohort study based on
fracture at any location
HR 2.1 (1.8-2.4)
controls matched by age
40 patients with a diagnosis
Prospective cross-sectional Dual energy X-ray densitometry, Risk of hip fracture
3.5 times greater in
et al. (55)
of CD in adulthood
Risk of major
Marsh III on I-II.
osteoporotic fracture 1.34 times greater
(lumbar, femoral neck, in Marsh III on I-II
forearm and shoulder)
CD: Coeliac disease; OR: Odds ratio; RRI: Relative risk increase; HR: Hazard ratio.
CD has been associated with low BMD since its very
first descriptions. Osteomalacia in children with CD is now
an exceptionally rare finding; unfortunately, the same can-
not be said for osteoporosis and osteopenia, which occur
in 40 % of patients diagnosed in adulthood and determine
a variable increase in the risk of bone fracture, leading to
lower quality of life. Changes in the epidemiology of CD
make low BMD screening by bone density scans more rel-
evant for adult coeliacs. Subjects with villous atrophy or
laboratory values suggestive of malnutrition at the time of
CD diagnosis may derive greater benefit from bone density
The gluten-free diet is also the basis of low BMD treat-
ment among coeliacs, and is sufficient in younger patients.
In adults with low bone mass, however, it must be supple-
mented with calcium and vitamin D. Although specific stud-
ies are lacking, bisphosphonates might also provide an
effective first line of treatment for adult coeliac patients
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