JOURNAL OF BONE AND MINERAL RESEARCH Volume 21, Number 9, 2006 Published online on June 19, 2006; doi: 10.1359/JBMR.060609 © 2006 American Society for Bone and Mineral Research
Intervertebral Disc Degeneration Can Predispose to Anterior Vertebral Fractures in the Thoracolumbar Spine Michael A Adams,1 Phillip Pollintine,1 Jon H Tobias,2 Glenn K Wakley,1 and Patricia Dolan1
ABSTRACT: Mechanical experiments on cadaveric thoracolumbar spine specimens showed that intervertebral disc degeneration was associated with reduced loading of the anterior vertebral body in upright postures. Reduced load bearing corresponded to locally reduced BMD and inferior trabecular architecture as measured by histomorphometry. Flexed postures concentrated loading on the weakened anterior vertebral body, leading to compressive failure at reduced load. Introduction: Osteoporotic fractures are usually attributed to age-related hormonal changes and inactivity. However, why should the anterior vertebral body be affected so often? We hypothesized that degenerative changes in the adjacent intervertebral discs can alter load bearing by the anterior vertebral body in a manner that makes it vulnerable to fracture. Materials and Methods: Forty-one thoracolumbar spine “motion segments” (two vertebrae and the intervertebral disc) were obtained from cadavers 62–94 years of age. Specimens were loaded to simulate upright standing and flexed postures. A pressure transducer was used to measure the distribution of compressive “stress” inside the disc, and stress data were used to calculate how compressive loading was distributed between the anterior and posterior halves of the vertebral body and the neural arch. The compressive strength of each specimen was measured in flexed posture. Regional volumetric BMD and histomorphometric parameters were measured. Results: In the upright posture, compressive load bearing by the neural arch increased with disc degeneration, averaging 63 ± 22% (SD) of applied load in specimens with severely degenerated discs. In these specimens, the anterior half of the vertebral body resisted only 10 ± 8%. The anterior third of the vertebral body had a 20% lower trabecular volume fraction, 16% fewer trabeculae, and 28% greater intertrabecular spacing compared with the posterior third (p < 0.001). In the flexed posture, flexion transferred 53–59% of compressive load bearing to the anterior half of the vertebral body, regardless of disc degeneration. Compressive strength measured in this posture was proportional to BMD in the anterior vertebral body (r2 ⳱ 0.51, p < 0.001) and inversely proportional to neural arch load bearing in the upright posture (r2 ⳱ 0.28, p < 0.001). Conclusions: Disc degeneration transfers compressive load bearing from the anterior vertebral body to the neural arch in upright postures, reducing BMD and trabecular architecture anteriorly. This predisposes to anterior fracture when the spine is flexed. J Bone Miner Res 2006;21:1409–1416. Published online on June 19, 2006; doi: 10.1359/JBMR.060609 Key words: vertebra, fracture, osteoporosis, mechanics, intervertebral disc degeneration, senile kyphosis
INTRODUCTION
V
ERTEBRAL DEFORMITY IS an important and growing cause of pain and disability in elderly people, often manifesting as senile kyphosis or “dowager’s hump.”(1) Deformity arises from various types of vertebral fracture, but the most typical is the anterior wedge fracture of a thoracolumbar vertebral body,(2) which can occur “spontaneously” or after some minor incident such as opening a window.(3) Such fractures are conventionally explained in terms of systemic factors that affect BMD in elderly people,
The authors state that they have no conflicts of interest.
such as reduced concentration of circulating sex hormones(4) and reduced physical activity.(5) However, this “conventional wisdom” does not explain why some genetic predisposition to osteoporosis can be independent of BMD.(6) Nor does it explain why the anterior vertebral body should be affected so frequently and in so characteristic a manner. Cancellous BMD is known to show regional variations, being higher posteriorly then anteriorly,(7) but currently there is no explanation for this. It seems that local mechanical factors must play a part in senile kyphosis, and to understand these, it is necessary to appreciate that the vertebral body does not function in isolation. In fact, it is compressed by the adjacent interverte-
1
Department of Anatomy, University of Bristol, Bristol, United Kingdom; 2Rheumatology Unit, University of Bristol, Bristol, United Kingdom.
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ADAMS ET AL.
FIG. 1. Diagram of spine motion segments with degenerated intervertebral discs (IVD) in the upright posture (left) and in a flexed (stooped) posture (right). The thickness of the arrows indicate how much of an applied compressive force is resisted by the anterior half of the vertebral body (VB), the posterior half of the vertebral body, and the neural arch (NA). In the presence of disc degeneration, flexing forward transfers loading from the neural arch to the anterior vertebral body.
bral discs, and it shares with the neural arch the task of resisting compressive force acting down the long axis of the spine.(8,9) Our recent work has shown that age-related degenerative changes in intervertebral discs cause them to concentrate loading on to the anterior region of the vertebral body when the spine if flexed.(10) In upright postures, however, degenerated discs concentrate more load on to the posterior half of the vertebral body.(10,11) Moreover, severe disc degeneration leads to a loss of disc height and a major transfer of compressive load bearing to the neural arch whenever the spine is upright. In extreme cases, >80% of the compressive force acting on the spine is resisted by the neural arches,(8) so that the vertebral body (and especially its anterior half) are substantially “stress-shielded” (Fig. 1). We hypothesize that altered load sharing in spines with degenerated intervertebral discs leads to a redistribution of bone mass, so that the anterior vertebral body becomes vulnerable to fracture when loaded in flexed (stooped) postures.
MATERIALS AND METHODS Nineteen human thoracolumbar spines 62–94 years of age (mean, 79 years) were collected from our postmortem room within 72 h of death and stored in sealed plastic bags at −20°C. Younger spines were excluded to minimize agedependent effects. Subsequently, spines were defrosted and dissected into 41 “motion segments” (two vertebrae and the intervening disc and ligaments). All spinal levels between T9–T10 and L5–S1 were represented, as follows: two at T9– T10, two at T10–T11, eight at T11–T12, eight at T12–L1, four at L1–L2, seven at L2–L3, six at L3–L4, three at L4–L5, and one at L5–S1. Lateral radiographs were taken, and intervertebral disc height was measured to the nearest 0.2 mm using calipers. Average disc height was calculated as the average height of the anterior annulus, nucleus, and posterior annulus. More than one specimen was used from each spine to
conserve a valuable resource, and the rationale for selecting which levels to test was to obtain the maximum number of motion segments for this (and other) experiments while avoiding (1) intervertebral discs that were too narrow to allow accurate readings from the pressure transducer (see below), (2) discs with bridging osteophytes that prevented insertion of the pressure transducer, and (3) any vertebra with a fracture demonstrable on radiographs. Specimens were mounted in cups of dental plaster for loading on a computer-controlled hydraulic materials testing machine (Zwick-Roell, Leominster, UK) and subjected to a constant load of 300N for 15 minutes to expel some water from the disc and guard against the possibility of postmortem superhydration.(12) Each specimen was compressed with a force of 1500N, which is appropriate to represent stooped standing and sitting postures in living people.(13) The manner in which this force was distributed on each vertebral body was examined by pulling a miniature pressure transducer, side mounted in a 1.3-mmdiameter needle, along the sagittal midline diameter of the adjacent intervertebral disc.(14) In most regions of the disc, transducer output is approximately equal to the compressive stress acting perpendicular to the transducer membrane(15). “Stress” measurements were integrated over area to give the force acting on the anterior and posterior halves of the vertebral body.(10) These forces were subtracted from the applied 1500N to indicate the compressive force resisted by the neural arch. Validation tests showed that errors in these force measurements are 2–8%.(8) Measurements were performed with the specimens positioned to simulate two specific postures in life: forward flexed or stooped posture (4–6° of flexion, depending on specimen mobility)(16) and erect standing or upright posture (2° of extension).(17) The strength of each motion segment was determined by compressing it to failure at 2 mm/s while positioned in 4–6° of flexion. Loading was removed as soon as failure was evident and in all cases before the motion segment lost >5% in height. Strength was calculated as the force resisted at the elastic limit (when stiffness first decreases). After testing, motion segments were dissected, and disc morphology was assessed from digital photographs. The grade of disc degeneration was assigned on a scale of 1 (young nondegenerated) to 4 (severely degenerated) as described previously.(18,19) Individual vertebrae were sectioned using a band saw, as follows (Fig. 2). The neural arch was removed, and the left and right superior articular processes of the lower vertebra of each motion segment were cut from the adjacent laminae along the pars interarticularis. Volumetric BMD of the superior articular processes was calculated from BMC and volume. BMC was measured using a PIXImus DXA scanner (Lunar Corp., Madison, WI, USA), and volume was measured by a water immersion technique. In validation tests on bone from six vertebrae, BMC was found to correlate highly with ash weight (r2 ⳱ 0.987), and measurements of bone volume were reproducible to better than 5%. BMD of the neural arch was represented by the BMD of the specimens of superior articular processes, averaged for the left and right sides. BMD of the anterior and posterior halves of the vertebral body were
VERTEBRAL FRACTURES
FIG. 2. Sectioning of vertebrae after mechanical testing. After removal of the neural arch at the pedicles, 2-mm-thick slices of vertebral body were cut in the midsagittal and parasagittal planes. Each slice was cut into nine blocks for histology. Comparisons were made between anterior blocks (1,4,7) and posterior blocks (3,6,9).
similarly measured. Data on neural arch BMD are presented for only 33 specimens, because of extensive damage to the neural arch of some specimens that occurred during related tests to assess load sharing.(8) Vertebral bodies were cut into 2-mm-thick parasagittal slices, which were embedded in acrylic resin before being sectioned into nine equally sized blocks, three each from the anterior, central, and posterior regions of the vertebral body (Fig. 2). Each block was sectioned at 7 m for histomorphometric analysis using the OsteoMeasure system (OsteoMetrics, Atlanta, GA, USA). Histomorphometric parameters were calculated according to standard formulae(20) and assumed a plate model for trabeculae. Results are presented for the three anterior and three posterior blocks from vertebrae taken from a subset of 17 motion segments selected at random. Statistical associations between variables were examined using univariate linear regression, and differences in histomorphometric variables between anterior and posterior regions of the vertebral body were examined using matchedpair t-tests. The influence of disc degeneration, posture, and spinal level on spine load sharing and strength was assessed using ANOVAs.
RESULTS Disc degeneration influences load sharing Distribution of the 1500N compressive load between the three regions (anterior vertebral body, posterior vertebral body, and the neural arch) is indicated in Table 1. In this table, data from the 41 specimens were augmented by data from 23 motion segments tested previously(10) to provide statistically meaningful results for specimens with all grades of disc degeneration. Mixed factor ANOVAs were used to analyze how load bearing in each region was influenced by posture (within subjects), disc degeneration (between subjects), and spinal level (between subjects). Load bearing by the neural arch and by the anterior vertebral body were significantly affected by posture (p < 0.001 in both cases) and by grade of disc degeneration (p < 0.001 and p < 0.006, respectively), but neither was influenced by spinal level. Several interactions between posture and disc degeneration were significant, and posthoc tests showed that anterior ver-
1411 tebral body load bearing decreased most between specimens with grade 2 and grade 3 discs, whereas neural arch load bearing increased most between grades 3 and 4. In the upright posture, neural arch load bearing increased from 8% in specimens with nondegenerated grade 1 discs to 63% in specimens with grade 4 discs. Load bearing by the anterior half of the vertebral body correspondingly decreased from 43% to 10%, whereas load bearing by the posterior vertebral body showed little systematic variation with disc degeneration. Load bearing in flexed posture was less affected by disc degeneration: in all specimens, the neural arch resisted 1–7% and the anterior vertebral body resisted 53–59% of the applied compressive force. Effectively, disc degeneration caused the neural arch to “stress-shield” the anterior vertebral body in the upright, but not flexed, posture. Neural arch load bearing was inversely proportional to average disc height as measured from radiographs (r2 ⳱ 0.38, p < 0.001).
Load sharing influences BMD and architecture Regional measurements of BMD reflected the loadsharing results. Overall, mean values of BMD for the anterior and posterior halves of the vertebral body and for the neural arch were 0.182 ± 0.057, 0.254 ± 0.106, and 0.744 ± 0.217 (SD) g/cm3, respectively. The ratio of BMD in the neural arch relative to the (whole) vertebral body increased with increasing load bearing by the neural arch in upright posture (Fig. 3A). Within the vertebral body itself, the ratio of BMD in the anterior and posterior halves was proportional to the ratio of load bearing by these two regions in upright posture (Fig. 3B). Reduced BMD in anterior regions of specimens showing high neural arch load bearing was strikingly apparent from radiographs (Fig. 4). High neural arch load bearing in upright posture was weakly associated with increased BMD in the neural arch (p ⳱ 0.07, n ⳱ 33). Reduced loading of the anterior vertebral body after disc degeneration (Table 1) was associated with inferior cancellous bone architecture, as indicated by histomorphometric measurements. Table 2 compares the histomorphometric results for the anterior third of the vertebral body with the posterior third in a subset of 17 vertebrae. The anterior region had a 20% lower trabecular volume fraction (BV/ TV), 16% fewer trabeculae (Tb.N), and 28% greater intertrabecular spacing (Tb.Sp; all p < 0.001). BV/TV was significantly correlated with volumetric BMD in the anterior (r2 ⳱ 0.71, p < 0.001) and in the posterior (r2 ⳱ 0.75, p < 0.001) vertebral body. Load bearing by the anterior vertebral body in upright posture was proportional to BV/TV (r2 ⳱ 0.39, p < 0.007) and Tb.N (r2 ⳱ 0.41, p < 0.006) and inversely proportional to Tb.Sp (r2 ⳱ 0.23, p < 0.05) in this region. However, in the posterior half of the vertebral body, load bearing was unrelated to these histomorphometric parameters, and anterior–posterior differences in histomorphometric measurements were not significantly related to grade of disc degeneration. Reduced bone volume fraction and inferior architecture in anterior regions of vertebrae adjacent to degenerated discs were evident in both midand parasagittal sections (Fig. 5).
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ADAMS ET AL. TABLE 1. DISTRIBUTION OF AN APPLIED COMPRESSIVE FORCE OF 1500N BETWEEN THE NEURAL ARCH (N ARCH) ANTERIOR (ANT) AND POSTERIOR (POST) HALVES OF THE VERTEBRAL BODY (VB)
AND THE
Distribution (%) of applied compressive force Upright posture
Grade Grade Grade Grade
1 2 3 4
(n (n (n (n
⳱ ⳱ ⳱ ⳱
6) 11) 28) 19)
Flexed posture
Ant VB
Post VB
N Arch
Ant VB
Post VB
N Arch
43 ± 11 33 ± 16 19 ± 13 10 ± 8
48 ± 5 49 ± 12 48 ± 14 26 ± 16
8±8 19 ± 14 34 ± 17 63 ± 22
58 ± 5 59 ± 4 58 ± 16 53 ± 15
40 ± 5 36 ± 7 38 ± 16 40 ± 15
1±3 4±5 5±6 7±6
Mean values ± SD are shown for each grade of disc degeneration (n is the number of specimens). Evidently, vertebral load sharing in the upright posture depends greatly on the grade of disc degeneration.
FIG. 3. BMD in various regions of a vertebra reflects their loadbearing role. (A) The ratio of BMD in the neural arch compared with the vertebral body is proportional to load bearing by the neural arch in the upright posture (r2 ⳱ 0.21, p < 0.01). Severe disc degeneration (grade 4) is associated with high load bearing by the neural arch and relatively high BMD in the neural arch. (B) The ratio of BMD in the anterior to posterior vertebral body is proportional to the ratio of compressive load bearing in the two regions. (r2 ⳱ 0.52, p < 0.001).
BMD and architecture influence strength The average compressive strength of motion segments (tested in the simulated stooped posture) was 3017 ± 1207N. Strength was proportional to BMD for the whole vertebral body (r2 ⳱ 0.48, p < 0.001) and to BMD for the anterior half of the vertebral body (r2 ⳱ 0.51, p < 0.001). Strength was also related to regional variations in BMD as indicated by the ratio of BMD in the neural arch relative to the whole vertebral body: strength decreased by >50% as this ratio increased from 2 to 7 (Fig. 6A). Compressive
FIG. 4. Radiograph of motion segment that exhibited high (80%) load bearing by the neural arch in the upright posture. Note the apparently low BMD in the anterior vertebral body. When image density was optimized for the apophyseal joints, the spinous processes became invisible. Reproduced with permission.(8)
TABLE 2. HISTOMORPHOMETRIC PARAMETERS MEASURED FOR ANTERIOR AND POSTERIOR REGIONS OF THE VERTEBRAL BODY (FIG. 2)
BV/TV (%) Tb.Th (m) Tb.N (mm−1) Tb.Sp (m)
Anterior
Posterior
9.8 ± 2.2 75.1 ± 12.9 1.8 ± 0.8 719 ± 325
12.4 ± 3.2* 76.2 ± 14.2 2.1 ± 0.9* 561 ± 231*
Values represent mean ± SD for 17 specimens. * Significant differences between anterior and posterior (p < 0.001).
strength was inversely related to neural arch load bearing in the upright posture (Fig. 6B), suggesting good internal consistency of the data set. A two-factor ANOVA showed that grade of disc degeneration significantly influenced (decreased) compressive strength (p ⳱ 0.002) and that spinal level did not.
VERTEBRAL FRACTURES
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FIG. 5. Radiographs of sagittal plane slices of elderly L2 vertebral bodies adjacent to degenerated intervertebral discs: (A) midsagittal section, male, 81 years of age; (B) parasagittal (pedicle) section, female, 76 years of age. Anterior is shown on the left. Note the inferior trabecular architecture in the anterior region of both slices.
Dissection showed that compressive damage was confined to one of the two vertebrae of the motion segment (not both). Damage was unlikely to have had much influence on subsequent measurements of bone density or architecture because loading was removed at the initiation of damage. All measurements on damaged and undamaged vertebrae in each motion segment were similar to each other. Disc degeneration did not show a strong dependence on spinal level but tended to be more severe at L4–L5 and T9–T12.
DISCUSSION Summary of findings The results support our hypothesis: they show that intervertebral disc degeneration and narrowing is associated with altered load sharing in elderly spines; that altered load sharing is related to regional variations in BMD; and that regional variations in BMD are related to vertebral compressive strength when the spine is flexed.
Strengths and weaknesses of the study Statistical associations do not prove causality, and there is a danger of finding spurious correlations between factors that all change consistently but independently with age. However, the age dependency of our variables was minimized by studying only elderly spines, and the consistent and linear relationships between load sharing, regional BMD, and strength strongly suggest causality. Direct associations between altered load sharing and compressive strength and between measures of bone quantity (BMD) and cancellous bone architecture (BV/TV, Tb.N, and Tb.Sp) emphasize the internal consistency of the data. Some of the scatter in the results (e.g., in Figs. 3 and 6) could be caused by the variable presence and size of marginal osteophytes on the vertebral bodies and apophyseal joints: osteophytes would increase BMD measurements, but their influence on compressive load bearing is unknown, and may be slight.
Relationship to other studies Vertebral body fracture is already associated with disc degeneration. (21) Disc degeneration can be detected
FIG. 6. Compressive strength of motion segments (in simulated stooped posture) decreases as (A) the ratio of BMD in the neural arch relative to the vertebral body (VB) increases (r2 ⳱ 0.27, p < 0.001, n ⳱ 33) and (B) as neural arch (NA) load bearing increases (r2 ⳱ 0.28, p < 0.001, n ⳱ 33).
on X-rays from reduced height of the annulus fibrosus, which indicates internal or external collapse of the annulus lamellae. (Disc degeneration can not be inferred reliably from the height of the nucleus pulposus because apparent nucleus height can be boosted artificially by collapse of the central region of the adjacent vertebral endplates.) Disc degeneration, quantified from narrowing of the annulus, is proportional to thoracic kyphosis.(22) This same study reported that all vertebrae with a pronounced kyphotic deformity (>5 mm anterior height loss) had less than average disc height.(22) Some other clinical evidence does not suggest a strong causal link between disc degeneration and vertebral kyphosis, but the following confounding factors may explain this. First, as reviewed previously,(10) most of these clinical studies do not distinguish between anterior wedge fractures and biconcave fractures of the vertebral endplates. The former may be related to disc degeneration as discussed in this paper, but the latter may represent the effects of fluid pressure in nondegenerated discs.(14,23) Pooling both types of fracture would therefore obscure any relationship between disc degeneration and anterior wedge fractures. Second, vertebral osteoporosis (and fracture risk) is often assessed on the basis of whole vertebra BMD measurements (antero-posterior DXA, for example), even though these measurements are influenced by the presence of osteophytes and are insensitive to focal bone loss from the anterior vertebral body. It is well established that spinal degeneration involving disc narrowing and facet joint hy-
1414 pertrophy (possibly resulting from the high compressive load bearing associated with narrowed discs?) can strongly influence AP-DXA, causing vertebral body BMD to be overestimated.(24,25) More focused studies have reported that local alterations in vertebral architecture, especially in the anterior vertebral body,(26) are associated with agerelated degenerative changes in the adjacent discs. Local alterations in BMD and trabecular architecture would be expected to have a large effect on the mechanical properties of the vertebra as a whole, because an inhomogeneous distribution of trabecular bone can lead to inferior mechanical properties compared with a more homogenous distribution.(27) The trabecular histomorphometric parameters measured for the anterior and posterior thirds of the vertebral body (Table 2) correspond with those found by other investigators using the same plate model for trabeculae.(26) A number of studies have shown that trabecular BMD and architectural properties are inferior in the anterior compared with the posterior vertebral body(7,26,28,29) and that the mechanical properties of intervertebral disc and adjoining cancellous bone are interrelated.(26,29,30) However, this is the first study to quantify the relationship between abnormal load sharing in the spine caused by disc degeneration with inferior BMD and architecture of the anterior vertebral body.
Explanation of results Underlying mechanisms can be explained as follows. Intervertebral disc degeneration reduces the height of the annulus fibrosus, bringing the adjacent neural arches closer together so that they resist more of the compressive force acting on the spine. Experimental disc height loss of between 1 and 4 mm in cadaveric spines has been shown to increase load bearing in the apophyseal joints of the neural arch when the spine is positioned in the simulated upright posture,(9) and intradiscal pressure in living people falls greatly in the presence of severe disc degeneration,(13) suggesting a transfer of loading to the neural arch. The vertebral body (and, in particular, its anterior half) is effectively “stress shielded” (Table 1), and so loses BMD according to “Wolff’s Law” of adaptive remodeling of bone. The neural arch tends to gain BMD for similar reasons, but this effect is slight, possibly because of the increased errors in measuring BMD in small samples of neural arch, and also because old bone is generally less able to increase bone mass as lose it, in response to altered loading.(31) In this way, vertebrae in spines with degenerated intervertebral discs become adapted to altered load sharing in upright postures, which are maintained for most of the day. However, this leaves them unable to cope with flexion movements that immediately transfer >50% of the compressive force on to the anterior region of the vertebral body. In the presence of severe (grade 4) disc degeneration, flexion increases the compressive force applied to the anterior vertebral body by 430% (Table 1, bottom row), and the reduced mass and inferior architecture of bone in this region leads to greatly reduced vertebral strength (Fig. 6). Flexion causes smaller changes in loading when discs are less degenerated (Table
ADAMS ET AL. 1). In living people, the dangers of flexion are amplified by increased tension in the back muscles, which contract to counter the forward bending moment of the upper body. Muscle tension increases the overall compressive force on the spine by a factor of 2–3 in full flexion,(13,32) so that the compressive force applied to the anterior region of a vertebral body adjacent to a “grade 4” disc would increase by up to 1290% (3 × 430%) compared with upright posture. Vigorous movements or heavy lifting in this posture would increase the compressive force further.(32) This explanation assumes that vertebral bone adapts to forces acting in habitual upright postures, rather than in occasional flexion movements, but this is a reasonable assumption because animal experiments show that between 4 and 36 loading cycles per day are required to induce an adaptive remodeling response.(33) When this evidence is combined with other evidence that old bone has a reduced responsiveness to mechanical stimulation,(34,35) it justifies the speculation that many middle aged and elderly people will not bend forward far enough or often enough to protect against bone loss. Once formed, an anterior wedge fracture will increase spinal kyphosis and move the center of gravity of the upper body anteriorly, so that the back muscles must increase their activity to prevent spinal flexion. This would increase compressive loading of the deformed spine and may well cause kyphotic deformity to progress.(36) However, altered load sharing after disc degeneration explains the initiation of kyphotic deformity in a previously undamaged spine. Local mechanical influences do not provide a complete explanation for senile kyphosis. r2 values reported above indicate that 21–52% of variance in the variables considered are explained by the proposed relationships, not 100%. Also important are age-related (systemic) changes in the skeleton caused by alterations in sex hormones(4) and activity levels,(5) as well as genetic inheritance.(6,37) However, the results of this study suggest that local mechanical influences can exacerbate these changes, and in many individuals, the effect can be large (Fig. 6).
Unanswered questions and future research The results suggest novel possibilities for the prevention, early detection, and treatment of senile kyphosis. The dramatic loss in BMD from the anterior vertebral body in spines with degenerated discs could conceivably be slowed, or even reversed, by exercises that include repetitive flexion movements of the thoracolumbar spine. It may seem paradoxical to recommend flexion exercises to prevent senile kyphosis (and indeed the recommendation should not be made to those who already have anterior wedge fractures(38)), but it is consistent with the principles of adaptive remodeling, and the efficacy of such exercises can readily be tested.(39) Identification of those at risk for senile kyphosis may be improved by performing DXA scans in the sagittal plane(40,41) to detect exaggerated bone loss from the anterior vertebral body and to check whether this is associated with relatively high BMD in the neural arch and with evidence of severe disc degeneration. Finally, treatments for senile kyphosis such as vertebroplasty and kyphoplasty,
VERTEBRAL FRACTURES which involve the injection of bone cement into weakened vertebrae,(42,43) may benefit from more anterior placement of the cement within the vertebral body. Preliminary work has shown already that anterior placement helps to restore normal load bearing in motion segments.(44)
ACKNOWLEDGMENTS This study was funded in the United Kingdom by the BBSRC. PD was a Research Fellow of the Arthritis Research Campaign.
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Address reprint requests to: Michael A Adams, PhD Department of Anatomy University of Bristol Southwell Street Bristol BS2 8EJ, UK E-mail:
[email protected] Received in original form September 27, 2005; revised form April 10, 2006; accepted June 9, 2006.
