Arch Orthop Trauma Surg (2011) 131:1703–1710
DOI 10.1007/s00402-011-1355-9
B A S IC S C IEN C E
Biomechanics of vertebral compression fractures and clinical
application
Michael A. Adams · Patricia Dolan
Received: 23 March 2011 / Published online: 31 July 2011
© Springer-Verlag 2011
Abstract Local biomechanical factors in the etiology of
vertebral compression fractures are reviewed. The vertebral
body is particularly vulnerable to compression fracture
when its bone mineral density (BMD) falls with age. How-
ever, the risk of fracture, and the type of fracture produced,
does not depend simply on BMD. Equally important is the
state of degeneration of the adjacent intervertebral discs,
which largely determines how compressive forces are dis-
tributed over the vertebral body. Disc height also inXuences
load-sharing between the vertebral body and neural arch,
and hence by WolV’s Law can inXuence regional variations
in trabecular density within the vertebral body. Vertebral
deformity is not entirely attributable to trauma: it can result
from the gradual accumulation of fatigue damage, and can
progress by a quasi-continuous process of “creep”. Cement
injection techniques such as vertebroplasty and kyphopl-
asty are valuable in the treatment of these fractures. Both
techniques can stiVen a fractured vertebral body, and kyp-
hoplasty may contribute towards restoring its height. The
presence of cement can limit endplate deformation, and
thereby partially reverse the adverse changes in load-shar-
ing which follow vertebral fracture. Cement also reduces
time-dependent “creep” deformation of damaged vertebrae.
Keywords Vertebral compression fracture ·
Biomechanics · Osteoporosis
M. A. Adams (&) · P. Dolan
Centre for Comparative and Clinical Anatomy,
University of Bristol, Southwell Street, Bristol BS2 8EJ, UK
e-mail: M.A.Adams@bris.ac.uk
P. Dolan
e-mail: Trish.Dolan@bris.ac.uk
Introduction
Vertebrae are the bones most commonly fractured when
elderly people suVer from osteoporosis. Age-related loss of
bone mineral density (BMD) can largely be attributed to
systemic inXuences, including declining levels of sex hor-
mones, and decreasing levels of physical activity [1]. How-
ever, local mechanical factors are required to explain why
fracture so often aVects certain vertebrae, and in very spe-
ciWc ways. The purpose of this review is to analyse these
local mechanical factors.
The review begins with some details of functional anatomy
because later sections will show how patterns of vertebral
body fracture can be understood only in terms of load-
sharing between adjacent spinal structures. The Wnal sections
move away from the traditional concept of a ‘fracture’ to
consider how repetitive loading can cause fatigue damage
to vertebrae, and how high static loading can result in “creep”
deformity of the vertebral body, even in the absence of a
demonstrable fracture.
Functional anatomy of the thoracolumbar spine
Vertebral body
Sometimes, it is overlooked that the vertebral body is only
one component part of a much larger bone—the vertebra
(Fig. 1). The vertebral body resists the compressive force
acting down the long axis of the spine, although this func-
tion depends on age, posture, and loading history, as dis-
cussed below.
Resistance to compression is mostly attributable to the
dense network of trabeculae (Fig. 2, upper) because
removal of the outer shell of cortical bone does not
123
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Fig. 1 Lumbar vertebra, showing the relative size of the vertebral
body and neural arch. (Adapted from: The Biomechanics of Back Pain,
published by Churchill Livingstone [17])
Fig. 2 Upper microradiograph of a 5-mm thick para-sagittal section of
an elderly human vertebral body. Note the concave superior endplate,
osteophytes, and regional variation in trabecular density. Lower values
of optical density (a surrogate for BMD) for various regions of such
bone sections. Values are the mean (STD) for sections from 29 verte-
brae. Arrows indicate signiWcant diVerences between superior and infe-
rior regions. Adapted from Zhao et al. [6] with permission
weaken the structure greatly [2]. Calculations suggest that,
in osteoporotic vertebrae, the cortex resists 15% of the
compressive load close to the endplates, and 45% at mid-
body height [3]. The load-bearing role of the cortex
increases in old vertebrae, which lose bone faster from tra-
beculae than from the cortex (Fig. 2, upper). The anterior
cortex is thicker and less porous than the posterior [4],
possibly because it must resist higher forces during for-
ward bending movements.
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Arch Orthop Trauma Surg (2011) 131:1703–1710
Vertebral body trabeculae tend to be denser and more
plate-like in the posterior vertebral body compared with the
anterior [5–8]. Likewise, trabeculae are denser in the infe-
rior half compared with the superior half [6, 7] (Fig. 2,
lower) possibly because they are reinforced by trabecular
arcades from the pedicles.
Vertebral endplates
The endplates, which mark the boundary with the adjacent
intervertebral discs (Fig. 3) are thin plates of cortical bone,
perforated by many small holes which allow the passage of
metabolites from bone to the central regions of the avascular
discs [9]. These holes doubtless weaken the endplate, and
may explain why it is the most easily damaged structure in
the thoracolumbar spine. Endplate thickness is least in the
centre of the endplate (Fig. 2, upper) even though mechani-
cal loading from the disc is greatest here, so endplate thick-
ness clearly reXects a trade-oV between strength and
metabolic requirements of the disc nucleus [6]. The superior
(cranial) endplate is consistently thinner than the inferior
(caudal) endplate of the same vertebral body [5, 6, 10] and it
is supported by less dense trabecular bone (Fig. 2, lower).
This asymmetry could possibly be explained by the
Fig. 3 Lower diagram shows a lumbar motion segment comprising
two vertebrae and an intervertebral disc (IVD) linking the vertebral
bodies. The insets show how Xexed postures (right) disengage the
articular surfaces of the apophyseal joints, whereas upright postures
(left) cause them to be load-bearing. S, C shear and compressive forces.
Stars indicate where bone–bone contact can take place. (Reproduced
with permission from: The Biomechanics of Back Pain, published by
Churchill Livingstone [17])
Arch Orthop Trauma Surg (2011) 131:1703–1710
additional loading applied to the lower half of the vertebral
body by muscles attached to the neural arch [6]. Endplates
are thicker and stronger posteriorly than anteriorly [11].
The central regions of each vertebral endplate are cov-
ered, on the disc side, by a thin layer of hyaline cartilage.
This tissue, which is similar to articular cartilage, is only
weakly bonded to the bone [12, 13] and its mechanical
function appears to help in spreading compressive loading
from the disc on to the vertebral body [14] while preventing
the migration of soft nucleus material into the pores of the
bony endplate.
Neural arch
A vertebra is much more than a vertebral body: the poster-
ior neural arch (Fig. 1) usually contains more bone, and the
proportion of bone in the neural arch is likely to increase
substantially in old age [8]. The neural arch is essentially a
ring of (mostly) cortical bone which encircles the spinal
cord, and it has several projections or processes which
serve as attachment points for muscles and ligaments. Mus-
cle and ligament forces can cause the entire neural arch to
bend upwards or downwards by 2–3° relative to the body,
pivoting about the pars interarticularis [15]. In some indi-
viduals, the spinous processes can resist a proportion of the
compressive force acting on the spine [16], but generally,
any compressive load-bearing by the neural arch is attribut-
able to the apophyseal joints.
Zygapophyseal joints
These small synovial joints stabilise the spine in compres-
sion, and prevent excessive bending and translation (sliding
movements) between adjacent vertebrae [17]. The articular
surfaces are approximately vertical in the thoracic and
upper lumbar spine, but more oblique at L4–5 and L5–S1.
This explains why the lower lumbar apophyseal joints resist
»20% of the compressive force acting perpendicular to the
mid-plane of the discs, while at the upper levels they resist
only half as much [18]. During backwards bending move-
ments, direct extra-articular contact with the inferior lamina
can occur [19, 20], as indicated in Fig. 3. Following patho-
logical narrowing of the intervertebral disc, lumbar apophy-
seal joints can transmit more than 50% of the spinal
compressive force from one vertebra to the next [8, 21]. On
the other hand, Xexion movements greatly reduce load-
bearing by the neural arches [8, 18].
Spinal ligaments
Most intervertebral ligaments span adjacent neural arches
(Fig. 3), posterior to the centre of sagittal plane rotation
within the intervertebral discs, so their primary action is to
1705
prevent excessive lumbar Xexion. Ligament tension in Xex-
ion can increase compression of the anterior column of
discs and vertebral bodies by 100% or more, even for the
same applied compressive force [22].
Intervertebral discs
These Wbrocartilaginous structures are bonded to adjacent
vertebral bodies (Fig. 4), and their primary function is to
distribute compressive forces evenly on them, while allow-
ing small intervertebral movements. The soft nucleus pul-
posus enhances this load-distribution function, with the
encircling lamellae of the annulus Wbrosus holding the
nucleus in place (Fig. 4). The technique of stress proWlome-
try [23], which has been extensively validated [24, 25], has
shown that the nucleus normally behaves like a pressurised
Xuid [26]. The surrounding annulus is able to resist high
concentrations of compressive stress [26], as schematically
shown in Fig. 4, even though it must exhibit a tensile
“hoop” stress to resist nucleus pressure.
With increasing age and degeneration, nucleus pressure
falls (both in vitro [26] and in vivo [27]) and stress concen-
trations increase in the annulus, as shown in Fig. 4. In
young non-degenerated discs, the whole interior region of
the disc behaves like a bag of Xuid, with an outer “skin” of
annulus only 2–4 mm thick. In older discs, the size of the
central hydrostatic region shrinks to that of the anatomical
nucleus, and small stress concentrations can be seen in the
annulus, usually posterior to the nucleus. In degenerated
discs, whether young or old, the central hydrostatic region
is small or absent, and high irregular stress concentrations
develop in the annulus. In severe degeneration, the disc
loses height, and compressive load is transferred increas-
ingly to the neural arch [28].
Mechanisms of vertebral compression fracture
This discussion concerns compression fractures, which usu-
ally aVect the vertebral body only. The compressive force
on the spine acts down the long axis of the spine, perpen-
dicular to the mid-plane of the intervertebral discs. It arises
from gravity, and from tension in the muscles of the back
and abdomen [29]. If traumatic injuries involving shear,
bending and torsion are included, then a much wider range
of fractures can be sustained [30].
It is convenient to categorise vertebral compression frac-
tures as shown in Fig. 5 [31], and the likely mechanism leading
to each type of fracture must be considered separately. How-
ever, many cadaveric studies have shown that the vertebral
body endplate is the “weak link” of the lumbar spine [32–35],
and it seems likely that some degree of endplate disruption
occurs in all types of vertebral compression fracture [36].
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1706 Arch Orthop Trauma Surg (2011) 131:1703–1710

Fig. 4 Right mid-sagittal sec-

tions through human lumbar
intervertebral discs, anterior on
left. These discs can be charac-
terised as young adult (top), old
but non-degenerated (middle),
and young and degenerated
(bottom). Left schematic repre-
sentation of the distribution of
compressive stress across the
mid-sagittal diameter of similar
discs to those shown on the
right. Note that degenerated
discs have a decompressed
central region, and high-stress
concentrations acting on the
surrounding annulus.
(Reproduced from Adams et al.
[67] with permission.)

“Biconcave” fractures Compressive overload usually fractures the cranial

Young intervertebral discs press evenly on their adjacent ver-
tebrae, in all postures, as the whole structure behaves like a
water-bed (Fig. 4). In middle age, however, only the central
nucleus pulposus exhibits a true hydrostatic pressure [26],
and this acts on the weak central region of the vertebral end-
plates. The annulus, in comparison, applies vertical compres-
sive stresses directly on to the relatively strong vertebral
cortices. Under these circumstances, the central region of the
endplates bulge into their vertebral bodies when the spine is
compressed [35, 37–39]. In young spines, vertical deXections
of the central endplate can exceed 0.5 mm without any dam-
age being sustained [38], and higher deformations are likely
with increasing age because of reduced trabecular support. If
loading becomes excessive, endplates will fracture and
become permanently deformed. Fracture can be diYcult to
visualize on radiographs [36], and in cadaveric specimens it
is sometimes necessary to press on the bone to detect the Wne
line of fracture running through the endplate or trabecular
bone [38]. Even in the absence of overt fracture, nucleus
pressure could probably cause vertebral endplates to slowly
develop a permanent and smooth concave shape by the pro-
cesses of bone creep and/or fatigue damage, as described
below in “Fatigue failure of the vertebral body” and “Gradual
“creep” deformation of vertebrae”.
endplate Wrst, both in vivo and in cadaveric experiments
[6, 36]. This is because it is thinner and weaker than the
caudal endplate (see above). Also, the cranial endplate is
less well supported by its adjacent trabecular bone
(Fig. 2). Often, however, the processes described earlier
result in both endplates bulging into the vertebral bodies
with increasing age [40, 41]. When these processes are
particularly marked, the deformity is referred to as a
“biconcave fracture” (Fig. 5 middle). Discs adjacent to
such fractures often have a full height, especially in the
nucleus, suggesting only moderate (if any) degenerative
changes within them.
In a minority of cadaveric specimens, small quantities of
soft nucleus pulposus are expressed vertically through a
damaged endplate to form an intraosseous herniation, often
referred to as a “Schmorl’s node”. Schmorl’s nodes are
commonly observed in living people [42], and tend to be
more irregular in older specimens with reduced BMD [39].
“Anterior wedge” fractures
Anterior wedge fractures are the most common vertebral
fractures, especially in elderly people and near the thoraco-
lumbar junction [31, 43]. They involve collapse of the ante-
rior vertebral body cortex together with a wedge-shaped

123
Arch Orthop Trauma Surg (2011) 131:1703–1710
Fig. 5 Three types of vertebral compression fracture: anterior wedge
(top), biconcave (middle) and crush (bottom). (Reproduced from Rao
and Singrakhia [43] with permission.)
region of trabecular bone behind it (Fig. 5 upper). The
cause of anterior wedge fractures is loss of bone from ante-
rior trabeculae and endplate, as described earlier, so that
this region of the vertebra is abnormally weak.
The underlying cause of anterior weakening appears to
be “stress shielding” of the anterior vertebral body by the
neural arch, following intervertebral disc narrowing [8].
Cadaveric experiments indicate that when the spine is posi-
tioned in an upright or lordotic posture, severe disc degen-
eration and narrowing result in 63% of the spinal
compressive force being resisted by the neural arch, with
only 10 and 26% being resisted by the anterior and poster-
ior halves (respectively) of the vertebral body and disc [8].
This in itself would lead to weakening of the anterior verte-
bral body, but not fracture. The real problem arises when
the spine is Xexed: even moderate Xexion disengages the
neural arches (Fig. 3) and concentrates more than half of
the applied compressive force on to the weakened anterior
vertebral body [8].
This explanation of anterior wedge fracture assumes that
vertebral BMD adapts to forces acting in habitual upright
postures rather than in occasional Xexion movements, but
this is consistent with animal experiments that show that 36
loading cycles per day are required to induce an optimal
adaptive remodelling response [44]. This, in combination
with the reduced responsiveness to mechanical stimuli of
old compared with younger bone [45, 46] suggests that
1707
many elderly people will not bend forwards far enough, or
often enough, to protect against bone loss from the anterior
vertebral body.
“Crush” fractures
Vertebral endplate damage causes an immediate and sub-
stantial reduction in pressure in the nucleus pulposus of the
adjacent disc [47], and concentrates compressive stress on
to the annulus (Fig. 4) and neural arch. Disc degeneration
has a similar eVect [26]. This explains why load-bearing by
the vertebral body cortex generally increases with age [48,
49]. If moderate spinal Xexion disengages the apophyseal
joints [28], as indicated in Fig. 3, then compressive over-
load can result in a crush fracture that primarily involves
the vertebral body cortex (Fig. 5 lower). Therefore, a crush
fracture is most likely to occur in a vertebral body adjacent
to a disc with a decompressed nucleus, and when the spine
is Xexed enough to ensure that the vertebral body is not
stress-shielded by the neural arch. If the crush fracture is
associated with relatively Xat endplates, then it can be
assumed that nucleus decompression arose from prior
degenerative changes in the disc [26, 27]. Alternatively, if
the endplates are concave, then the nucleus decompression
may have arisen from prior endplate damage, or creep.
In young spines, compressive trauma can sometimes
cause “burst fractures” which have a similar appearance to
crush fractures, but with more radial outwards displacement
of the cortex.
Fatigue failure of the vertebral body
Old vertebrae can lose strength to such an extent that they
fracture during the normal activities of daily living [50]. In
such cases, fracture may indicate the end of a gradual pro-
cess of accumulating microdamage [51] resulting from
numerous similar exertions. The process of cumulative
“fatigue failure” of the vertebral body has been investigated
in human cadaver spines [52–54], and Table 1 shows how
the force required to cause fatigue failure decreases as the
number of loading cycles increases. Typically, compressive
strength is reduced by 30–40% if 10 loading cycles are
applied and by 60–70% if 500 cycles are applied. Fatigue
damage is similar in appearance to that which occurs during
a single loading cycle [52].
Evidence that fatigue failure occurs in living bones
comes from the observation of individual fractured and
healing trabeculae in many cadaveric vertebral bodies [55].
In living people, the accumulation of fatigue damage would
be opposed by the continual process of bone turnover, so a
likely timescale would be days or weeks rather than years,
and it would depend on the person’s age. A plausible
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1708
Table 1 Values indicate the probability (expressed as a %) of com-
pressive failure if a spinal motion segment is loaded for the speciWed
number of loading cycles at the speciWed relative load
Relative Number of loading cycles
load (%)
10 100 500 1,000
60–70 10 55 80 95
50–60 0 40 65 80
40–50 0 25 45 60
30–40 0 0 10 20
20–30 0 0 0 0
Relative load is the actual compressive load expressed as a percentage
of the load required to cause compressive failure in a single loading
cycle. Data from Brinckmann et al. [52]
scenario for fatigue failure of a vertebral body might be an
elderly man performing several hard days’ gardening at the
start of a new season.
Gradual “creep” deformation of vertebrae
Many elderly people diagnosed with fractured or deformed
vertebrae do not recall any preceding incident [50], and
their radiographs may reveal no clear fracture plane. This
suggests that vertebrae can deform gradually under con-
stant load by some quasi-continuous ‘creep’ mechanism.
Bone is certainly a ‘viscoelastic’ or ‘anelastic’ material [56,
57], and repeated loading of small bone samples leads to a
‘residual deformation’ that recovers slowly, if at all [58].
Recently, studies on whole human vertebrae from elderly
cadavers have conWrmed that they deform gradually under
constant loading at physiological load-levels (Fig. 6), pro-
vided that the BMD is low [59]. Since BMD and trabecular
density tend to be lower anteriorly than posteriorly (see
above), creep is greater anteriorly, and the vertebral body
develops a slight but measurable anterior wedge deformity.
Typically, a creep test (at 21°C) lasting 2 h results in an
anterior wedge deformity of 0.1° [59]. Small bone samples
do recover from creep, but only very slowly, and it may
take 20 times as long as the period of loading [58]. Whole
vertebrae may not fully recover [59], or may not do so suY-
ciently before the next period of sustained loading. The
underlying mechanisms of bone creep are unknown, but
could involve Xuid Xow within canaliculi, slipping at the
cement lines which separate adjacent osteons, or prolifera-
tion of microcracks. The latter is enhanced when bone is
deformed slowly [51].
Creep deformations in vitro are increased by more than
500% if the vertebra has suVered minor damage, even if
that damage is so slight that it can barely be detected on
radiographs [60]. The rate of creep remains substantially
higher in anterior regions of the vertebral body, exaggerat-
123
Arch Orthop Trauma Surg (2011) 131:1703–1710
5,000
100
90
70
25
10
Fig. 6 Creep deformation and recovery curves (after smoothing) for a
typical 2 h creep test on a cadaveric motion segment (Fig. 3). Speci-
men: male, aged 80 years. The three graphs show vertical compressive
strains (% deformation) in the posterior, middle and anterior regions of
the L2 vertebral body. Elastic (el), creep (cr) and residual strains (res)
are labelled for the anterior vertebral body. 10,000 microstrains
(strain) = 1% deformation. (Reproduced from Pollintine et al. [59]
with permission.)
ing any anterior wedging. This line of research is in its
early stages, but it appears that focal damage to trabecular
bone leads to increased loading on adjacent tissue, which
then undergoes local plastic deformation [57], if its BMD is
suYciently low. This in turn throws increased loading on to
adjacent bone, so that a progressive deformity develops.
It is diYcult to extrapolate from these cadaver experi-
ments to living humans because the rate of creep decreases
with time (Fig. 6) and may eventually approach equilib-
rium. Also, creep could conceivably be faster, or recover
faster, at body temperature. Prospective studies on patients
are required to determine the inXuence of creep, and accel-
erated creep, on vertebral deformity in later life.
Clinical application: vertebral augmentation
Many of the adverse mechanical consequences of vertebral
compression fracture can be countered, or reversed, by
cement augmentation techniques. Injecting ‘cement’ into
the vertebral body of fractured vertebrae (vertebroplasty)
increases pressure in the nucleus of the adjacent disc,
restores compressive load-bearing to the disc and vertebral
body, and reduces load-bearing by the neural arch [61]
(Fig. 7). These mechanical eVects may be inXuenced by
factors such as vertebral BMD [61, 62], fracture severity
[61, 63] and the degree of degeneration in adjacent discs
[61]. They also depend on the volume of injected cement,
with smaller volumes acting to equalise stress in the disc,
but larger volumes being required to increase compressive
stiVness and to reduce loading of the neural arch [64]. Our
Arch Orthop Trauma Surg (2011) 131:1703–1710
Fig.7 Distribution of compressive stress across the antero-posterior
diameter of an intervertebral disc, before and after the adjacent verte-
bral body was fractured. Note that cement injection (vertebroplasty)
largely restored normal load-bearing to the damaged disc-vertebral
body unit. A, P anterior, posterior. IDP intradiscal pressure. (Repro-
duced from Luo et al. [61] with permission.)
latest (unpublished) research suggests that the accelerated
rate of creep deformation following fracture may be
reversed or slowed by vertebroplasty. However, the ability
of cement augmentation to restore vertebral height remains
uncertain. Kyphoplasty, which involves elevating the end-
plate using an inXatable bone tamp before the injection of
cement, may have some potential in this respect [65]
although there is only limited clinical evidence to support
this [66].
ConXict of interest The authors declare that they have no conXict of
interest.
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