From: Yonsei Med J. 2009 Oct 31;50(5):624-9

Facet tropism is defined as asymmetry in both the facet joint angles of the lumbar and lumbosacral regions. For many years, the effect of facet tropism on the development of intervertebral disc degeneration has been debated. However, the specific details regarding the effects of facet tropism on the development of degenerative disc disease remains as the subject of debate. Most of the previous facet tropism studies have focused on the relationship between facet tropism and lumbar disc herniation.

The role of facet tropism in the pathogenesis of lumbar degenerative disc disease is not fully understood Currently, controversy exists surrounding the question of whether or not any significant relationship exists between facet tropism and the development of disc or facet joint degeneration. Additionally, the relationship between facet tropism and degenerative spondylolisthesis and translational segmental motion is highly controversial.

In the current study, the authors attempted to evaluate the effect of facet tropism on disc and facet joint degeneration. Additionally, the relationship between facet tropism and changes in translational segmental motion was investigated.

Facet tropism is defined as asymmetry between the left and right facet joint angles of the lumbar spine. Asymmetry in the orientation of the zygapophyseal joint surfaces is not uncommon, with estimates of its occurrence at 10-70.5% of the population. Our study revealed an incidence of facet tropism in 35% of the spinal units which were taken into consideration. Facet tropism is most common at L5-S1, followed by L4-L5.

The criteria for determining facet tropism have varied greatly, although the actual definition of facet tropism is asymmetry between the right and left facet joints. In the lumbar spine, the majority of facet joints vary by less than 7° in orientation between the two sides. Noren et al. defined facet asymmetry as a bilateral angle difference greater than 5°. In other biomechanical studies, facet asymmetry was defined as a difference in facet angles greater than 1-10° or one SD. Grogan, et al. divided facet joint tropism into three distinct classifications. When the orientation differed from one side to another by more than 7°, the facet joints at that level were defined as having tropism. Moderate tropism was defined as a difference of 7° to 15° between the orientation of the joints (one SD from the mean difference) and severe tropism was defined as a difference of more than 15° (two SDs from the mean) between the two sides. For the current study, the authors defined facet tropism to be bilateral angular asymmetry greater than 7°.

The angular difference inherent to facet joint tropism causes biomechanical issues. By definition, facet joint degeneration exists when one joint has more coronal orientation than the other. Farfan and Sullivan emphasized the importance of coronally facing facet joints upon the development of lumbar disc herniations. Coronally facing facet joints offer little resistance to shear intervertebral force, so that the joints tend to rotate toward the side of the more coronary facing facet joint, possibly leading to additional rotational stress on the annulus fibrosus. Loback, et al. showed that facet joint asymmetry is found more likely on the side of the coronally facing facet joint. When tropism was present, the motion segment was found to have a tendency to rotate towards the more oblique joint when axial loads were applied. This asymmetric axial rotation caused by tropism can place additional torsional loads on the intervertebral discs which can lead to intervertebral disc injury and degeneration. This biomechanical mechanism was used to describe the development of lumbar disc herniation, disc degeneration, and degenerative spondylolisthesis associated with facet tropism. Some studies have claimed that lumbar facet joint tropism does not accelerate degeneration of the facet joints. For the current study, the authors chose to investigate facet tropism and some of the findings associated with lumbar degenerative disc disease, including disc degeneration, facet joint degeneration, and spondylolisthesis (translational segmental motion).

The role of facet tropism in the pathogenesis of disc degeneration is a contested issue. Boden, et al. and Vanharanta, et al. reported no significant correlation between facet tropism and disc degeneration. However, Noren, et al. concluded that the existence of facet tropism can increase the risk of disc degeneration. Additionally, Dai reported that a significant correlation existed between facet joint tropism and the degree of disc degeneration in patients with degenerative spondylolisthesis. In the present study, no significant correlation was observed between facet joint tropism and disc degeneration at L3-L4, L4-L5, or L5-S1. However, a higher (but not statistically significant) incidence of highly degenerated discs at L4-L5 was observed within the facet tropism group.

Grogan, et al. concluded that lumbar facet joint tropism does not accelerate facet joint degeneration. They reported no significant differences in facet joint degeneration between facet joints with and without tropism. However, there are many limitations associated with this study. It was based on a small number of specimens (21 cadavers) and an even smaller number of lumbar facet joints exhibiting facet tropism (10 out of 104 lumbar facet joints). Additionally, this study did not take the level, where the tropism occurred, into consideration. Our current study included L3-L4, L4-L5, and L5-S1 facet joints belonging to 300 living participants and our findings were found to be similar to Grogan et al.’s at L3-L4 and L5-S1. However, at L4-L5, a significant correlation between facet joint tropism and facet joint degeneration was observed. Based on the fact that L4-L5 experiences the most segmental flexion and extension within the lower lumbar spine, this result suggests that the existence of facet tropism within highly mobile lumbar segments could affect the development of facet joint degeneration.

Berlemann, et al. reported that facet joint asymmetry does not seem to play a major role in the development of degenerative spondylolisthesis. However, Dai found that facet joint tropism was a predisposing factor for the development of degenerative spondylolisthesis. The present study found no association between facet tropism and translational segmental motion (such as vertebral slippage) within the lumbar spine. Our results indicate that facet tropism has no major association with the development of degenerative spondylolisthesis.

Previous reports have shown that facet orientation has a significant association with degenerative spondylolisthesis. Additionally, some of these studies reported that, in patients with degenerative spondylolisthesis, the transverse plane of facet joints was more sagittally oriented. All of these studies found that individuals with larger facetjoint angles, relative to the coronal plane (more sagittal orientation of facet joint), exhibited a higher incidence of degenerative spondylolisthesis. Although facet orientation was not taken into consideration for this study, the authors believe that it is an important element for understanding all of the factors that lead to the development of spondylolisthesis, and that this topic should be investigated further.

Another interesting factor to take into consideration is the existence of facet joint tropism within normal spines. This raises questions as to the root causality of facet joint tropism. Facet joint tropism could be caused by an inborn characteristic of the human spine, as a result of mechanical stresses on the spine (i.e., asymmetric loading of the human spine) or as a consequence of existing spinal deformities (i.e., scoliosis). Noren, et al. documented that subjects with lumbar degenerative disc disease had a higher incidence of facet joint tropism than the normal population. The nature of the relationship between facet joint tropism and degenerative changes within the lumbar spine remains a controversial topic. Essentially, there are two sides to this debate, one advocating that facet tropism leads to degeneration and the other claiming that certain degenerative statuses (i.e., degenerative spondylolisthesis) lead to facet tropism. Our results show that, at active functional spine units, facet tropism partially influences the development of facet joint degeneration. This seems to give legitimacy to the theory that facet tropism can lead to facet joint degeneration, although further investigation into the relationship between facet tropism and facet joint degeneration is necessary.

From: Spine (Phila Pa 1976). 2009 Oct 16

The effect of postural change on degenerative lumbar discs was quantified using novel kinematic magnetic resonance imaging. The purpose is to describe the bulging of degenerative intervertebral lumbar discs in vivo subjected to different postural loads using a novel kinematic magnetic resonance imaging.

Symptomatic lumbar disc degeneration is a leading cause of pain and disability throughout the world. Over 70% of US citizens will experience a debilitating episode of low back pain. Earlier reports of degenerative disc changes are cadaver studies or are performed with recumbent MRI that eliminates the functional effects of gravity and muscle power. Little data are available on the behavior of degenerative intervertebral discs in vivo under physiologic loads.

A total of 513 patients obtained kMRI. Disc bulging beyond the intervertebral space was quantified during upright neutral, flexion, and extension imaging. The degree of intervertebral disc degeneration was correlated using the Pfirrmann Classification. Moderately degenerated intervertebral discs (grade III and IV) demonstrated greater bulging than mildly degenerated discs (grade II). Severely degenerated discs (grade V) also showed a trend toward greater bulging, but this was not significant. Grade I discs at all levels moved posteriorly in flexion and anteriorly in extension when compared to neutral posture. However, mild to severe (grade II-V) degenerative discs behaved differently in response to postural loads. Extension resulted in significant posterior bulging, while flexion did not demonstrate obvious anterior derangement.

Disc bulging increases with the severity of disc degeneration. Grade I discs demonstrate the expected sagittal migration in response to postural load. However, more degenerative discs behave less predictably, and spine extension may result in significant posterior disc bulging. Degenerative changes in the intervertebral disc significantly affect the kinematic patterns under postural load in vivo. Kinematic magnetic resonance imaging is a useful tool to quantify the kinematic behavior of degenerative intervertertebral discs.

Tags: degenerative, lumbar, discs,, symptomatic, lumbar, disc, degeneration,, postural, load

From: Spine (Phila Pa 1976). 2009 Oct 15;34(22):2389-94

This article investigates the effects of cervical disc herniation on kinematics at adjacent vertebral motion segments. Kinetic magnetic resonance imaging is an alternative method to conventional MRI, which allows evaluation of the cervical spine in a more physiologic, weight-bearing position, and acquisition of images in flexion, extension, and neutral alignment. Kinetic magnetic resonance imaging has previously been used to evaluate the effects of disc degeneration on cervical kinematics. A total of 407 patients with neck pain without prior history of surgery were evaluated using kinetic magnetic resonance imaging. Translational motion, angular variation, and disc height were measured at each segment from C2-C3 through C7-T1. Other factors including the degree of disc degeneration, age, gender, and vertebral segment location were analyzed in order to determine any predisposing risk factors for segmental instability adjacent to disc herniations.

Spinal levels above the disc herniation exhibited, on average, a 7.2% decrease in translational motion per mm of disc herniation, without significant change in angular motion. Levels below the herniation demonstrated a 5.2% decrease in angular motion per mm of disc herniation without significant change in translational motion. The degree of disc degeneration had no significant effect on adjacent level motion. Disc herniation had no significant impact on disc height at adjacent levels, although disc degeneration correlated with decreased disc height above and increased disc height below.

Although disc height, translational motion, and angular variation are significantly affected at the level of a disc herniation, no significant changes are apparent in adjacent segments. This study indicates that herniated discs have no effect on ROM at adjacent levels regardless of the degree of disc degeneration or the size of disc herniation, suggesting that the natural progression of disc degeneration and adjacent segment disease may be separate, unrelated processes within the cervical spine.

Tags: cervical, disc, herniation,, cervical, kinematics,, disc, degeneration

From: J Orthop Sci. 2009 Sep;14(5):602-10

The authors conducted a prospective long-term follow-up study to assess associations between magnetic resonance imaging (MRI) findings and changes in clinical symptoms, as well as factors relating to the prognosis of symptoms. A total of 133 patients with acute whiplash injury between 1993 and 1996 participated in this follow-up study. They underwent neurological examinations by spine surgeons and second MRI scans of the cervical spine were obtained. They also filled out a questionnaire regarding cervical symptoms and the accident details. The items evaluated by MRI were (1) a decrease in the signal intensity of the intervertebral disc; (2) anterior compression of the dura and the spinal cord; (3) posterior disc protrusion; (4) disc space narrowing; and (5) foraminal stenosis. Relations between the presence/absence of degenerative changes on MRI, accident details, and patients’ symptoms were assessed by calculating the adjusted odds ratio.

Progression of some degenerative changes was recognized on MRI in 98.5% of the 133 whiplash injury patients, and clinical symptoms diminished in more than a half of the 133 patients. There were no statistically significant associations between MRI findings and changes in clinical symptoms. The prognosis for neck pain tended to be poor after accidents with double collisions (rear-end collision followed by frontend collision) and accidents with serious car damage. The prognosis for stiff shoulders tended to be poor in women; and the prognosis for numbness in the upper extremities tended to be poor after accidents with serious car damage. This study demonstrated that progression of degenerative changes of the cervical spine on MRI was not associated with clinical symptoms during the 10-year period after whiplash injury.

Tags: cervical, spine,, whiplash,, whiplash, injury,,

From: Clin Orthop Relat Res. 2009 Sep 18

Neck pain is one of the most common chronic conditions affecting quality of life and sometimes causing disability in adults. Most chronic neck pain is the result of degeneration of the intervertebral discs in the cervical spine. An intact end plate cartilage is critical for normal disc functions, as the major nutrient supply of the discs is diffused through the end plates. Pathological changes in end plate cartilage are closely related to disc degeneration and thus to cervical spondylopathy. Prevention and reduction of lesions to the vertebral end plate are high research priorities.

IL-1beta may play an important role in intervertebral disc degeneration. This being the case, inhibiting IL-1beta could provide a therapeutic approach for reducing or preventing disc degeneration. Muscone reportedly relieves pain and suppresses inflammation. Therefore, the authors asked whether muscone, a potent antiinflammatory agent, could reduce proinflammatory cytokines in vitro (end-plate cartilage cultures) and end-plate degeneration in vivo (a rat model that induces intervertebral disc degeneration). In vitro, muscone reversed IL-1beta-induced upregulation of IL-1beta, tumor necrosis factor alpha, cyclooxygenase 2, inducible nitric oxide synthase, matrix metalloproteinase 13, aggrecanase 2, and nitric oxide and downregulation of Col2alpha1 and aggrecan. Pretreatment with muscone (6.25, 12.5, 25 mumol/L) inhibited the IL-1beta-induced phosphorylation of extracellular signal-regulated kinases 1/2 and c-Jun N-terminal kinase in a dose-dependent manner. In vivo, muscone inhibited the expression of prostaglandin E2, 6-keto-prostaglandin F1alpha, IL-1beta, and tumor necrosis factor alpha and recovered the structural distortion of the degenerative disc. The findings suggest muscone is a promising agent for treating intervertebral disc degeneration through its antiinflammatory effects.

From: Spine (Phila Pa 1976). 2009 Sep 14

An in vivo study of the effects of mechanical loading on transport of small solutes into normal human lumbar intervertebral discs using serial postcontrast magnetic resonance imaging (MRI) to investigate the influence of a sustained mechanical load on diffusion of small solutes in and out of the normal intervertebral disc.

Diffusion is an important source of disc nutrition and the in vivo effects of load on diffusion in human intervertebral disc remains unknown. Forty normal lumbar discs (on MRI) in 8 healthy volunteers were subjected to serial post contrast (Gadoteridol) 3 Tesla MRI in 2 phases. In phase 1 (control), volunteers were scanned at different time points – precontrast and 1.5, 3, 4.5, 6, and 7.5 hours postcontrast injection. In phase 2, 1 month later, the same volunteers were subjected to sustained supine loading for 4.5 hours. MRI scans were performed precontrast (preload) and postcontrast (postloading) at 1.5, 3, and 4.5 hours. Their spines were then unloaded and recovery scans performed at 6 and 7.5 hours postcontrast. In house software was used to analyze images.

Repeated-measures ANOVA and pairwise comparisons at different time points in the central region of the loaded disc compared to the unloaded discs revealed significantly lower signal intensity ratios indicating reduction in transport rates for the loaded discs. Signal intensity ratioscontinued to rise in loaded disc for 3 hours into recovery phase, whereas unloaded discs at the same time point showed a decrease.

Sustained supine creep loading (50% body weight) for 4.5 hours retards transport of small solutes into the center of human IVD and it required 3 hours of accelerated diffusion in recovery state for loaded disc to catch-up with diffusion in unloaded discs. The study supports the theory that sustained mechanical loading impairs diffusion of nutrients entering the disc and quite possibly accelerates disc degeneration.

From: Arthritis Res Ther. 2009 Aug 20;11(4):R126. [Epub ahead of print]

The human intervertebral disc is an avascular and aneural tissue comprising a central gelatinous region (the nucleus pulposus), surrounded by a fibrous ring of highly organised collagen fibres (the annulus fibrosus). The extracellular matrix of the nucleus pulposus is rich in type II collagen and proteoglycans, predominantly aggrecan, which produces a highly hydrated matrix capable of withstanding the loads experienced within the spine. This extracellular matrix is constantly being remodelled in a process driven by the constituent nucleus pulposus cells.

During intervertebral disc degeneration there is an imbalance in the normal homeostatic mechanisms, which favours matrix catabolism and leads to a loss of disc height,
coupled with ingrowth of both nerves and blood vessels into both the annulus fibrosus and nucleus pulposus. The authors have previously demonstrated that this ingrowth of nerves into the degenerate intervertebral disc is associated with low back pain. While low back pain is multifactorial, studies have shown that this debilitating condition affecting around 80% of adults at some stage of life is associated with intervertebral disc degeneration in approximately 40% of cases. Indeed in a recent study by Cheung et al (2009) it has been shown that there is a significant association of lumber disc degeneration imaged by MRI with low back pain.

The nucleus pulposus of the normal human intervertebral disc is an avascular and aneural environment, comprising of chondrocyte like cells embedded within an extracellular matrix rich in proteoglycans and collagens. This matrix is continuously remodelled in a process controlled by the nucleus pulposus cells and closely regulated by anabolic growth factors and catabolic cytokines. In intervertebral disc degeneration there is disregulation in this finely balanced homeostatic matrix turnover mechanism, leading to an increase in catabolic processes over anabolic matrix formation. Over time this results in breakdown of matrix, until the disc loses both height and function and in a large proportion of cases there is innervation and initiation of the pain response which leads to low back pain.

Matrix metalloproteinases (MMPs) are known to be involved in the degradation of the nucleus pulposus during intervertebral disc degeneration. This study investigated MMP-10 (stromelysin-2) expression in the nucleus pulposus during intervertebral disc degeneration and correlated its expression with proinflammatory cytokines and molecules involved in innervation and nociception during degeneration which results in low back pain.

Human nucleus pulposus tissue was obtained at post-mortem from patients without a history of back pain and graded as histologically normal or degenerate. Symptomatic degenerate nucleus pulposus samples were also obtained at surgery for low back pain. Expression of MMP-10 mRNA and protein was analysed using real time PCR and immunohistochemistry. Gene expression for proinflammatory cytokines IL-1 and TNF-alpha, nerve growth factor and the pain associated neuropeptide Substance P were also analysed. Correlations between MMP-10 and IL-1, TNF-alpha and nerve growth factor were assessed along with nerve growth factor with Substance P.

MMP-10 mRNA was significantly increased in surgical degenerate nucleus pulposus when compared to post-mortem normal and post-mortem degenerate samples. MMP-10 protein was also significantly higher in degenerate surgical nucleus pulposus samples compared to post-mortem normal. IL-1 and MMP-10 mRNA demonstrated a significant correlation in surgical degenerate samples, while TNF-alpha was not correlated with MMP-10 mRNA. Nerve growth factor was significantly correlated with both MMP-10 and Substance P mRNA in surgical degenerate nucleus pulposus samples.

MMP-10 expression is increased in the symptomatic degenerate intervertebral disc, where it may contribute to matrix degradation and initiation of nociception. Importantly, this study suggests differences in the pathways involved in matrix degradation between painful and pain free intervertebral disc degeneration.

This study has demonstrated, for the first time, increased MMP-10 expression in the symptomatic degenerate intervertebral disc when compared to non-degenerate or asymptomatic degenerate intervertebral disc . The correlation of MMP-10 with IL-1 and nerve growth factor, combined with the correlation between nerve growth factor and Substance P in symptomatic degenerate intervertebral disc’s suggests differences in the catabolic pathways between painful and pain free intervertebral disc degeneration. While this study focused on gene and protein expression profiling, it emphasizes the importance of MMP-10 in symptomatic intervertebral disc degeneration and highlights that a more detailed investigation into these pathways, including analysis of enzyme activities is required to better understand the underlying pathogenesis.

From: Med Hypotheses. 2009 Jul 23. [Epub ahead of print]

Modic changes are bone marrow and endplate lesions visible in magnetic resonance imaging (MRI). They are regarded as a part of degenerative disc disease and associated with low back pain. And severe disc degeneration was occurred more in the patients with Modic changes. But there is still no study to analyze the relationship between Modic changes and intervertebral disc degeneration. The authors hypothesize that Modic changes are the possible causes and promotion of lumbar intervertebral disc degeneration. And there are three possible mechanisms for this hypothesis:

A structural cause: Modic changes make cartilaginous material easier in extruded disc herniations, to destroy the structure of intervertebral disc and inhibit the absorption of the disc.

A biomechanical cause: Modic changes alter the mechanical loading distribution on disc, to initiate a series of disc disruption and inhibit the self-recovery of the disc.

A nutritional cause: Modic changes destroy the vascular architecture in vertebral endplate and block the most important metabolism pathway between vertebrae and disc.

Perspectives:

(1) Find out procedures to cure Modic changes may be an important breakthrough for disc degenerative disease.

(2) Treatment of Modic changes may be a critical step of biotherapy for disc degeneration disease.

From: Matrix Biol. 2009 Jul 5. [Epub ahead of print]

Degeneration of intervertebral discs and articular cartilage can cause pain and disability. Risk factors include genetic inheritance and age, but mechanical loading also is important. Its influence has been investigated using miniature pressure transducers to measure the distribution of compressive stress (force per unit area) within loaded tissue. The technique quantifies stress concentrations, and detects regions that behave in a fluid-like manner.

Intervertebral discs demonstrate a central fluid-like region which normally extends beyond the anatomical nucleus pulposus so that the whole disc functions like a “water bed”. With increasing age, the fluid region shrinks and pressure within it falls. Stress concentrations appear in the surrounding anulus fibrosus, with location depending on posture. Stress concentrations become large in degenerated discs, and are intensified by sustained loading or injury. Articular cartilage never exhibits an internal fluid pressure: stress gradients and concentrations normally occur within it, and are intensified by sustained loading.

Excessive matrix stresses can cause pain and progressive damage. They also inhibit matrix synthesis and stimulate production of matrix degrading enzymes. In this way, injury to chondroid tissues can initiate a ‘vicious circle’ of abnormal matrix stresses, abnormal metabolism, weakened matrix, and further injury, which explains many features of their degeneration.

Intervertebral discs and articular cartilage facilitate movement and load-transfer in joints. In both of these chondroid tissues, a sparse population of cells maintains an extensive matrix of proteoglycans and collagen, and although the tissues are mostly devoid of blood vessels and nerves, both give rise to pain and disability when affected by degenerative changes. Matrix biology research involving both types of cartilage show some striking parallels, and considerable overlap. There is increasing
recognition that, in both tissues, matrix function and failure depend on complex interactions between genetic inheritance, cell biology, and the mechanical environment.

The intensity of mechanical loading acting within chondroid tissues can be described in terms of stresses and pressures. Stress is the force per unit area acting in or on a solid, and usually varies with location and direction. Pressure is the force per unit area acting in a fluid, and is normally the same in different directions and locations because static fluids have negligible rigidity, and simply deform (flow) to equalise pressure within them. It has been known for many years that the nucleus pulposus of healthy intervertebral discs has such a high water content that it behaves like a fluid, and exhibits a hydrostatic pressure, even though it is sometimes capable of sustaining stress gradients. In contrast, the disc’s anulus fibrosus, and articular cartilage, are fibrous solids with considerable rigidity.

Internal pressures and stresses in chondroid tissues are important for two reasons. High stress concentrations and stress gradients have the potential to disrupt the internal tissue architecture, leading to progressive structural failure as seen in advanced disc degeneration and osteoarthritis (OA). Secondly, cell metabolism is sensitive to stresses and pressure in the surrounding matrix. For example, rounded chondrocytes in articular cartilage and nucleus pulposus increase matrix synthesis in response to moderate hydrostatic pressure, but decrease their synthesis and produce more proteases if the stresses become too high or low. Fibroblast-like cells of the outer anulus respond to cyclic stretching but not to hydrostatic pressure. If cells are dispersed in a soft artificial matrix prior to loading, then realistic cell deformations can be achieved at stress levels less than 1% of those experienced in a living tissue, and yet it is unclear which mechanical signals affect the cells most: stress, or strain (which is % deformation). It is apparent therefore that mechanically-driven failure of chondroid tissues, and cell-mediated responses to mechanical loading, both depend on the nature and distribution of stresses in the extracellular matrix.

Although great efforts are being made to understand how cells respond to their mechanical environment, much less attention has been given to characterising the environment that the cells are responding to. This is unfortunate, because the application of the wrong type or magnitude of loading will lead to very different cell responses, and potentially misleading results.

The internal mechanical environment of chondroid tissues can be studied conveniently using finite element (FE) models. These were first developed to characterise stresses and strains in engineering structures made of simple elastic materials but with complex architecture. Unfortunately, intervertebral discs and articular cartilage have simple structure, but are made from complex fibrereinforced materials which require the models to make many simplifying assumptions. Consequently, FE models of such structures must be validated against experimental measurements before their predictions can be trusted. Experiments are also required to answer fundamental questions such as “how does fluid expulsion under load influence the ability of chondroid tissues to distribute stress evenly on the subchondral bone?” and “how does tissue injury influence stress distributions?”

From: J Manipulative Physiol Ther. 2009 Jun;32(5):352-7

Throughout the course of the day, the spinal intervertebral discs display viscoelastic creep properties that determine an individual’s overall stature. These properties were demonstrated by Tyrrell et al who used in vivo stadiometry measurements to detect 19.3 mm (1.1% of stature) variation in height between first arising and the end of the day.

Contributions to the total diurnal stature loss from structures other than the intervertebral disc are minimal. Kanlayanaphotporn et al used stadiometer measurements to assess the contribution of soft tissue structures below the sacrum and concluded that these structures accounted for 19% of the height change during the first 5 minutes of sitting. Based on these findings, stadiometry is considered to provide an accurate measure of spinal height changes after various loading conditions.

The 2 primary methods of measuring spine height changes are magnetic resonance imaging (MRI) and stadiometry. Stadiometry has been shown to be a valid and reliable tool to assess spinal height when compared to objectifiable measures made from MRI. Stadiometry assessment has advantages over MRI in terms of costs, use in clinical setting, as well as the ability to measure subjects that simultaneously sustain compressive loads of the trunk.

Several authors have assessed the effects of postures and different compressive loads on spinal height using stadiometry. Kourtis et al used stadiometry to identify increased height associated with prolonged hyperextension in lying, where a gain in intervertebral disc height after this activity was confirmed using MRI. The mean disk height gain from intervertebral discs T11 to L5 measured by MRI after extension lying was 2.1 mm, whereas the average total spine height gain measured by stadiometry was 5.2 mm. The results consistently demonstrated an increase in participant height when measured using MRI and stadiometry after a position of extension lying that followed a seated loaded position. Similar findings were reported by Magnusson et al who indicated sustained extension lying of 20° for 20 minutes provided the optimal impact on the increase of spine height.

Although previous studies have assessed the effects of extension postures on spine height, no previous investigation has assessed the effects of flexion postures. Therefore, the purposes of this study were 3-fold: (1) to determine if the authors test protocol using a commercially available stadiometer demonstrated findings consistent with prior laboratory-based protocols; (2) to determine if hyperextension in the prone position and trunk flexion in the supine position caused increased spine height after sustained loading; and (3) to compare the effects of hyperextension in the prone position and trunk flexion in the supine position on spine height changes after a period of sustained loading.

The authors clinically applicable protocol using a commercially available stadiometer confirmed the findings of previous research by Kourtis et al that reported loss of trunk height associated with loaded and unloaded sitting. Kourtis et al used MRI to measure changes of intervertebral disc height associated with loading and unloading of the spine. The research methods of the current study matched the methodology and population of Kourtis et al who reported mean changes (−5.03 mm) in spinal height similar to the changes recorded in this study (−3.24 mm). These findings are consistent with previous investigations including 4.28 mm height loss, 3.07 and 3.55 mm height loss, and 3.85 mm height loss recorded after 5 minutes of sitting in young adults.

This is the first reported investigation to assess the effect of trunk flexion in the supine position on spine height using a stadiometer measurement protocol. Magnusson et al suggested that increased lumbar intervertebral disc hydration occurred as a result of load transfer from the lumbar intervertebral disc to the zygapophyseal joints during lumbar extension postures. The authors findings suggest that trunk flexion in the supine position provides similar increase in spine height as those obtained through extension postures. Therefore, controlling the effects of gravity on the intervertebral diskc through unloading the spine seems to bear greater influence on increased spine height and hydration of the discs than the directionality (flexion or extension) of the position of the spine.

No significant differences were found between sexes for any of the experimental conditions, suggesting that sex and body frame were not associated with variability in spine height changes. These results are in agreement with previous findings, which indicated no effect on spine height changes associated with sex, suggesting that trunk height changes associated with various recovery positions can be generalized for both sexes in asymptomatic young adults.

Spine height measurements, using stadiometer protocols, are largely dependent on lumbar intervertebral disc hydration. Kourtis et al using both stadiometer and MRI to assess the effects of various positions on trunk height, reported similar results for extension recovery positions under both techniques. This reflects the intervertebral discs’ ability to imbibe fluid during periods of unloading and lose water with loading, translating into trunk height changes detected using stadiometer measurements. Under normal conditions, the lumbar intervertebral disc is able to imbibe large quantities of water. With intervertebral disc degeneration, the ability to bind water and maintain hydration is diminished. Positions that temporarily aid in the recovery of spine height may help offset these consequences and provide ergonomic applications.

Therapeutic interventions for the management of low back pain can be assessed in terms of intervertebral disc hydration level reflected through spine height changes. This includes the evaluation of various positions and exercises to prevent or treat back pain, the use of traction and manual therapy techniques as well as exercises in the aquatic setting. Future studies should include patients with various conditions such as nonspecific low back pain, lumbar radiculopathy, and lumbar intervertebral stenosis. Determining if a correlation exists between intervertebral disc hydration levels reflected in spine height measures using stadiometer protocols and patient symptoms may provide additional management strategies for the management of low back pain.