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Back to Physician Literature THE AGING SPINE
RICHARD L. ZIPNICK, MD, JOSEF GOREK, MD, JOHN P. KOSTUIK, MD, CAMERON B. HUCKELL, MD ANN N.
SIEBER, RN, MSN, HELEN SIGWALD, RN, ONC VIVEK MOHAN, BSFrom the Spinal Division Department of Orthopaedic Surgery The Johns Hopkins Hospital Baltimore, Maryland
Reprint requests to:
John P.
Kostuik, MD Department of Orthopaedic Surgery The Johns Hopkins University School of Medicine 601 N. Caroline Street, Room 5232 Baltimore, MD 21287-0882
About 20% of all Americans will be older than 65 by the year 2000. Twelve percent will be older than 85. Orthopedic practice sees a higher proportion of the elderly due to the
prevalence of musculoskeletal complaints. In today's orthopedic practice, 25% of the patients are 65 and older. The Census Bureau projects that the 65 and older group will double from 33 million to 65 million in 2030
while the younger age groups stay the same. Physicians will deal with more people who are experiencing intellectual failure, immobility, instability, incontinence, insomnia, and iatrogenic problems.
Spinal
stenosis and vertebral osteoporosis are expensive problems. The annual cost of treating all cases of osteoporosis is $10 billion. The cost for treating vertebral osteoporosis alone is 40% of the total, or $4 billion
annually.
Humans are mechanically constructed to live to the age of 35 and after that are on borrowed time. Major therapeutic discoveries have prolonged life expectance to 75 years. Although the discovery of
antibiotics in 1928, insulin in 1921, cortisone steroids in 1935, and folliculin or estrogen in 192430
have helped maintain the integrity of the musculoskeletal system, bone mineral density continues to decline after the age of 30. Weaver and Chambers measured trabecular bone strength on cubes frorn'the central region of the lumbar vertebral body from a total of 150 autopsy cases. They found an increase in strength to the age of 30 and then a linear, agerelated decline.
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FIGURE 1. Lateral radiograph shows the anterior shift in the center of gravity in a severely kyphotic elderly woman with
an osteoporotic: T6 compression fracture. |
Peak bone mass is obtained by age 30, after which all individuals lose a small amount each year. In the initial year
after menopause or oophorectomy, 5% of cancellous bone mass is lost and bone mass gradually decreases for 5 years. Half of all women older than 65 have radiographic evidence of osteoporosis, and 90% are affected by
age 75. Back pain, deformity, and loss of body height result from the anterior shift in the center of gravity.13 Most of the total height loss is due to disc degeneration, but vertebral wedging and
collapse also contribute to the problem.23 Figure I shows the anterior shift in the center of gravity in a severely kyphotic elderly woman with an osteoporotic T6 compression fracture.
The axial skeleton can change size or shape or simply renew itself without changing shape. Each of these processes employs different mechanisms with different controlling influences. Bone modeling
differs from remodeling. Bone modeling is the process by which the overall shape of bone is changed in response to physiologic and mechanical influences. Vertebrae may widen or change in axis with
the removal or addition of bone. The increase in vertebral width is caused by the addition of new consolidated bone layers at the periosteal surface while removal of bone occurs at the center of a
vertebra." Spinal stenosis and osteoporosis, the two most common results of aging, biomechanically exist on the same degenerative continuum. Osteophytes function to increase the surface area to
support loads (Fig. 2).
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FIGURE 2. Anteroposterior (A) and lateral (B) radiographs in an 82-year-old woman with chronic low back pain
show osteophytes that developed as a result of spinal instability, causing spinal canal stenosis and new-onset radicular pain. |
FIGURE 3. Vertebral widening (black line) occurs as a result of spinal instability after disc degeneration.
Resultant wedging and fracture can lead to spinal stenosis; (arrow) and leg pain. |
The area moment of inertia is increased by adding more consolidated trabecular bone to the vertebral periphery. Simultaneously, the
vertebral centrum is resorbed. The bone shifts from the center to the periphery in efforts to better resist stress. Vertebral widening (Fig. 3) occurs as a result of spinal instability after disc degeneration, which
causes back pain. Leg pain occurs from neuroforaminal stenosis. The vertebral centrum resorbs and is subject to wedging and fracture, which may further cause back pain.
The human vertebral body is constructed to provide maximum strength with minimal mass. In young individuals, the load-bearing capacity of a lumbar vertebra is 1,000 kg. The intervertebral discs,
which distribute local stresses over the vertebral endplates, are even stronger. With age, internal trabecular mass and architecture change due to modeling. These changes start in the center (the vascular
region) and progress superiorly and inferiorly. Age-related endplate thinning occurs, as does thinning of the "cortical" rim due to endosteal bone resorption. The increase in cross-sectional area is
due to new periosteal bone formation and osteophyte formation. A 10-fold reduction in bone strength occurs with aging.This changes the strong vertebral body of a young person from 1,000 kg to one with a
load-bearing capacity of 80-150 kg in an elderly person. The vertebral changes result from disc degeneration, which occurs first because stress is no longer distributed by the flat inelastic cushions. With
bone loss, the structural distribution of strain within the material is critical to where fracture or stress concentration may occur.6 Osteoporotic vertebral fragility and spinal stenosis simultaneously
result.
Trabecular network disruption with age is caused mainly by perforation of horizontal supporting struts. Spinal reconstruction deals with trabecular bone mechanics. Cancellous, or trabecular, bone
exists in the spine and pelvis.5 The entire axial skeleton is trabecular bone. Even the bony shell (ring and endplates) around the vertebral bodies does not resemble cortical bone histologically. The shell
should rather be characterized as condensed trabecular bone.12 The pelvis is not exempt from osteoporotic trabecular failure. Delayed pelvic ring fractures occur in 6% of patients older than 50 following
long instrumented lumbosacral spine fusions, but patients younger than 50 have no risk even when fused from above Ll to the sacruM.44 Fractures in the elderly clearly involve trabecular bone.28
A fracture in one trabecular region precipitates a second fracture elsewhere.
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FIGURE 4. Representation of an osteoporotic compression fracture. |
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With compressive deformation of 15%, the horizontal trabeculae fail at their base attachment to the vertical trabeculae by a cantilever
beam mechanism14 (Fig. 4), allowing the vertical trabeculae to slide past each other as the endplates approximate. These are brittle fractures of normally ductile structures. As is normal in all brittle
fractures, the cracks are linear and perpendicular to the tensile stresses. The vertical elements sustain internal inicrodarnage but retain their shape and general architecture. Cracks grow gradually
until critical size is reached, at which point a sudden brittle fracture occurs, such as when a person steps off a curb. In older adults, it is the tensile residual stresses from modeling that occurs; in younger
adults, the tensile applied stresses cause fractures.
In men, compression tests on whole vertebral bodies have shown the decline in bone strength to be much more pronounced than the
decline in mass. Since a fivefold decrease in vertebral strength occurs with aging, a 30% increase in vertebral cross-sectional area occurs from ages 20-80.11 Bone is shifted from the vertebral center to
its periphery to support normal loads. Peak bone mass for men is 25% higher than in women and is simply due to the fact that men have larger vertebral bodies. Although the structure is different, the
density and material properties are identical. After age 25, the vertebral bodies and the femoral neck are the only sites in the normal skeleton where load-bearing trabecular bone is surrounded by hemopoietic marrow.
12 Bone is removed from these vascular regions and transported to the outer trabecular shell. The pedicle's outer diameter increases both from aging and iatrogenically when
screw-induced microfracture callous forms. The most functional age-related changes occur in overall vertebral volume and shape.
This chapter describes the effects of aging in the human spine and
shows that osteoporosis and spinal stenosis occur simultaneously. Three of the most common spinal manifestations of aging are described: cervical spondylotic myelopathy, spinal stenosis, and osteoporosis.
CERVICAL SPONDYLOTIC MYELOPATHY
Cervical spondylotic myelopathy is the most common cause of spinal cord dysfunction in patients who are older than 50.40 The
disease is often overlooked, and the oversight of gait disturbance contributes to geriatric falls that result in hip and spine fractures and head injuries.
The initial lesion is intervertebral disc deterioration.
35 Loss of disc height approximates the vertebral bodies and uncovertebral joints of Luschka. Disc herniation occurs. Loss of disc height causes ligamentous laxity followed by vertebral body subluxation. The
diameter of the vertebral body increases as a result of reactive hyperostosis. The osteophytes compress spinal cord blood vessels and nerve tissue. The axis of rotation migrates to the stable spinal
segment-the facet joints. The facet joints then degenerate. Facet and uncovertebral joint osteophytes further compress the spinal cord and nerve roots. The ligamenturn flavurn becomes inelastic and
invaginates into the canal and compresses the cord. A developmentally narrow canal lowers the threshold at which the spinal cord is compressed and causes myelopathy.2
Five distinct syndromes exist that are characterized by degenerative radiographic and clinical signs of spinal cord compression:10 (1) lateral nerve root compression with radicular pain, weakness, or
paresthesia; (2) myelopathy with long tract signs and symptoms; (3) myeloradiculopathy combined with both root and long tract signs and symptoms, which is the most common form; (4) 70% cord tissue
vascular ischernia from anterior spinal artery compression with nonspecific motor and sensory deficits; and (5) anterior syndrome secondary to a posterior disc bulge during neck flexion impinging on
the anterior hom with painless upper extremity weakness and normal lower extremities. Progressive circumferential spinal canal and neuroforaminal encroachment occurs.
Patients with cervical spondylotic myelopathy also experience unsteady tandem walking with a stooped, wide-based jerky gait, poor balance, unsteady feet, and loss of manual dexterity. Bladder
incontinence is rare but can occur.10 Whitematter posterior column (funiculus gracilis) ascending necrosis and lateral tract (corticospinal tracts) demyelination occurs with white matter anterior column
sparing.3 Gray matter central cyst formation with anterior and posterior horn phagocytosis and gliosis occurs, as does dorsal nerve root atrophy. Less often, ventral nerve root atrophy occurs.
About 15% of patients treated nonoperatively with collar/brace immobilization; medications such as NSAIDs, muscle relaxants, and epidural steroids; and physical therapy will improve. About 85% have
persistent motor deficits without spontaneous regression.' The prevention of further progression is adequate reason to intervene operatively. Early operative decompression within the first year of
symptoms before irreversible neurologic loss can occur provides the best outcome. About 75% of patients will improve, 10% will worsen, and 15% will worsen or stay the same. II Patients older than 70 with
dense neurologic deficit and incontinence, medical illness, and depression have a poor prognosis; however, decompression to prevent further deterioration should be considered.
The results achieved with anterior or posterior decompression are comparable. The anterior approach is generally recommended when the myelopathy is caused by anterior compression at one or two
levels and in patients with kyphosis.41 The intervertebral disc and part of the adjacent vertebral bodies are removed, as are offending osteophytes, a herniated disc, and, if calcified, the posterior
longitudinal ligament. Nerve root decompression is limited by the vertebral arteries laterally. The decompression is generally followed by an autologous tricortical iliac crest arthrodesis. A long fibular strut
graft is used after three or more levels of decompression.4 Some Surgeons have reported good success with canal decompression without arthrodesis.18 Each fused interspace decreases the overall
spinal motion. Adjacent levels are subjected to more stress, and degeneration is accelerated. Grafts may collapse, extrude, or fail to fuse. The fusion rate decreases as the number of levels increases.17
The posterior approach is recommended for more than three levels of decompression and for patients who have developmental stenosis.11 Decompression involves laminoplasty or extensive laminectornies of
the third through sixth cervical vertebra, with the addition of appropriate foraminotornies for specific nerve root decompression when radiculopathy is present.18 After laminoplasty, patients lose
neck extension.
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FIGURE 5. The three-joint complex involved in spinal stenosis. |
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SPINAL STENOSIS
The most common cause of neurologic leg pain in older patients is spinal stenosis.11 The pathology
involves the three-joint complex (Fig. 5).
As in cervical spondylotic myelopathy, the intervertebral disc degenerates first. There is disc collapse with subsequent facet
arthrosis, both of which progressively narrow the neuroforamen and compress the nerve root. Ligamentous laxity causes vertebral subluxation and
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FIGURE 6. The axis of rotation, which is located at the stiffest part of the spine, initially resides in the
anterior column. However, after disc degeneration and segmental instability, the axis moves posteriorly into the facet joints, which are then subjected to abnormal loads and degenerate further
and cause spinal stenosis. |
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osteophyte formation, with resultant spinal stenosis (Fig. 6). Soft tissue compression occurs from the disc anteriorly and
the ligamenturn flavurn posteriorly. The neuroforamen is more narrowed with lumbar lordosis than with lumbar flexion. The patient prefers to sit and flex and not to stand and extend. Intrinsic nerve root venous outflow
obstruction produces neuroischemia and impairs circulation of cerebrospinal fluid. The site of neural compression may be centralcanal, lateral recess, neuroforamen, and combined." Spinal stenosis reflects
primarily degenerative disc and facets. Canal narrowing can be congenital, which lowers the threshold for compression. Stenosis results in dynamic compression in addition to static anatomic changes. 19
Later, spondylolisthesis occurs after disc degeneration and facets arthrosis with sagittal plane subluxation. Degenerative scoliosis results from disc collapse and can
cause ligamentous laxity and transverse plane translation and rotation. Figure 7 shows an example of spinal stenosis secondary to an L1 osteoporotic burst fracture and concomitant avascular necrosis.
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FIGURE 7. A, the L1 vertebra initially was intact. B and C, simultaneous progressive lower lumbar
instability (black arrows) and a progressive proximal osteoporotic compression fracture (white arrows) result in a "double crush" stenosis with severe low back and leg pain. |
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Little information exists about the efficacy of conservative treatment. Epidural steroids provide short-term relief only. Short-term
success rates for simple decompression are 85% but deteriorate with long-term surveillance. Predictors of high failure rates include long-term surveillance. Predictors of high failure rates include long-term follow-up,
cardiac disease and diabetes and use of more extensive decompression. Best results occur in patients with one or two levels of decompression without spondylolisthesis. Success occurs in 96% of patients after
decompression and fusion for concomitant degenerative spondylolisthesis, 44% with decompression alone. Whether improved results occur with the addition of hardware remains to be answered. 13
Initail treatment is symptomatic and includes NSAIDs and restriction of aggravating activities. Aerobic conditioning such as swimming and stationary bicycling are recommended. Instructions can be simplified
to include 30-minute activities three times per week.
Surgical decompression involves removal of compressing bone and soft tissues. Instability occurs after one total facet removal, either by
complete unilateral ablation or by 50% removal bilaterally. Prophylactic intertransverse process fusion is performed after extensive decompression. The results of decompression alone
without fusion are less favorable. Decompression combined with fusion has produced in excess of 50% better results than decompression alone. 17 Four years after decompression alone, 17%
of patients required redecompression because of recurrent stenosis and instability.20 Disc violation also may cause late instability.
OSTEOPOROSIS
Osteoporosis is the most common cause of spinal deformity and, because it occurs after intervertebral disc degeneration, is the most common cause of axial back pain in the elderly. Most osteoporotic
vertebral fractures are a result of failure under axial compression. Although these fractures are classically considered compression fractures, they frequently involve the posterior cortex and should
technically be called burst fractures (Fig. 8).
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FIGURE 8. L1 osteoporotic burst fracture with avascular necrosis and stenosis. |
Burst fractures cause stenosis, deformity, and pain, but compression fractures only cause deformity. About 30% of patients have radiographic
evidence of instability or spinal stenosis proximal to a previous spinal fusion when evaluated at an average of 30 years after fusion.26 Osteoporotic patients are more likely to develop a compression fracture
proximal to the fusion. Supra-adjacent vertebral failures are seen as early as 1 year after osteoporotic spinal fusion. Patients with previous scoliosis fusions may in postmenopausal life develop
adjacent osteoporotic fractures. Transition syndrome occurs above and below an instrumented fusion from disc degeneration (Fig. 9). Chapman et al. analyzed patients who developed fractures above or below a solid fusion.
7 Although the most significant cause was global malalignment caused by creating a hypolordotic or kyphotic lumbar spine, elderly osteoporotic patients
were at greatest risk, indicating a material contribution to proximal failure. The authors were surprised to find no distal transition syndromes at L5-S1 and a significant number of proximal junctional kyphoses at T1-T3.
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FIGURE 9. Thirty-eight years after spinal fusion to L4 for scoliosis, this 54-year-old woman complained of
pain in the low back and left leg. She lacked extension to neutral and had normal sacroiliac joints. Findings of sagittal imbalance (A and B) but only slight coronal imbalance (C and D) indicated the need
for revision surgery for the correction of flat back deformity. External views show asymmetry of the waist fold (D) and a lateral view (E). A discogram confirmed the source of back pain. Spinal stenosis
(black arrow in F), which also was present, caused the patient's complaint of left L5 radiculopathy. Subjacent degeneration below the level of fusion (G-I) required extension of the fusion to the sacrum by
anterior L5-S1 interbody fusion in addition to a posterior L4-5 closing wedge osteotomy and L5 decompression and fusion to the sacrum. |
Pelvic fractures that occur in adults older than 50 after long lumbosacral fusions are an example of increased subadjacent stress.
Pubic rami strains significantly increased during rotation maneuvers after instrumentation. Figures 9 and 10 show problems that developed in two patients who had previously undergone spinal fusion.
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FIGURE 10. Radiographs taken in 1993 (A) and 1995 (B) demonstrate progressive subjacent disc segment degeneration in a
38-year-old woman. She previously had a posterior spinal fusion with Harrington rod instrumentation for scoliosis, which resulted in a flat back deformity. The white arrows point to the lower end of the
fusion, and the black arrows point to the disc.. |
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FIGURE 11. Kyphyotic deformity and trunk imbalance associated with progressive bone loss (A) is modified surgically (B)
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Progressive bone loss is inevitable, and some patients experience the relentless occurrence of multiple vertebral fractures that result in
dramatic kyphotic deformity and severe postural problems (Figs. 11 and 12). Chronic back pain, stenosis, and associated degenerative disease occur. Kyphosis progression stops when the lower ribs begin
to impinge on the iliac wings (Fig. 11). This impingement is associated with local pain due to soft tissue and costal nerve irritation. Severe intractable pain is managed by costal nerve blocks.
Rib resection is strongly contraindicated.
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FIGURE 12A-D. Preoperative coronal and sagittal deformtity due to osteoporosis and scoliosis in an elderly woman with rib
impingement on her iliac wing and severely limited extension. |
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FIGURE 12E-H. Surgery to lift the patient's ribs off her pelvis with a posterolateral closing wedge osteotomy and fusion
led to restitution of sagittal imbalance and coronal correction. |
Scoliosis in elderly women (see Fig. 12) is a clinical marker for osteoporosis and compression fractures. Evaluation of an adult
scoliotic with bone biopsy may be necessary.16, 24 Osteoporotic vertebral fractures causing neurologic deficits are more common than has been previously appreciated. The initial presentation involves a
complaint of back pain only. The patients then acquire radicular pain and neurologic deficit up to 1 year after the initial fracture. The neurologic sequelae are related to the progressive onset of spinal
stenosis secondary to progression of angular deformity at the fracture site. The cause of further collapse may be biomechanical. Geometric malalignment predisposes a vertebra to further anterior compression.
Osteoporotic posterior fusion fatigue is really a geometric problem and not a material one. Additional vertebral fractures can occur after certain interventions that arrest bone loss or even produce significant
gains in bone mass. These observations suggest an important role for regional realignment and overall bone quality, which is operationally defined as the architectural and structural
characteristics. In addition to bone mass, these characteristics contribute to bone strength.19 Avascular necrosis also occurs (see Fig. 8), and its presence is greatly underestimated. Therefore,
anyone who sustains an osteoporotic fracture should be followed for a minimum of one year.
Spontaneous pain resolution may be expected in 2-10 weeks regardless of treatment. Ambulation is encouraged; studies of bed
rest in younger patients indicate that bone loss of up to 1% per week can be expected.21 Bracing is useful because the benefits of keeping the patient ambulatory may significantly outweigh the potential risks
afforded by stress shielding. However, deformity and stenosis persist because disconnected trabecular structures cannot be reestablished: there is no surface for ostcoblasts to work on, nor is there any
mechanical stimulation.34 Here, trabeculae are subject to random "walks through space" as a result of micromodeling. Nonsurgical treatment for osteoporosis has failed.
Surgical indications for osteoporosis include progressive painful deformity of kyphoscoliosis, neurologic deficits, and instability. Neurologic deficits and.instability are associated with stenosis.
Vertebral fixation using the holding power of the pedicle is best; however, advancing the screws to the anterior cortex and supplemental methylmethacrylate injection increases purchase.
PMMA supports instrumentation in bone.21,22 PMMA-augmented pedicle screws have doubled the pullout force even after the threads were stripped and reinserted.45
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FIGURE 13. A, an instrumented scoliosis correction uses the Harrington sacral bar cemented into the right iliac crest and
bar connectors dominoed to the formal posterior instrumentation. The L5 pedicle screws provide an antirotation effect, B, the anterior column support provided by a titanium cage (black arrow) is filled with
autogenous bone graft and fixed in compression by two 6.5-mm. titanium cancellous lag screws. The white arrow points to the Harrington sacral bar. |
The entirely trabecular sacrum represents a particular problem. The
choice is either to share load by installing anterior lumbar interbody grafts or to distribute load via multiple sacral fixation points.
The osteoporotic sacrum is most amenable to load sharing. However,
there are several sacral locations for instrumented purchase. At S1 the promontory or lateral alar mass is available. Bicortical purchase is recommended: anterior cortex perforation increases the holding
power by 50% and is safe at the midpoint since there are no vascular structures at this location. However, 1 cm. distal to the promontory, bone strength decreases by 50%. The iliosacral buttress of Jackson
intrasacral fixation secured with an oblique bicortical S1promontory screw decreases cantilever forces and makes this construct useful in the osteoporotic sacrum.
This is especially true for scoliosis correction if the iliac crests are bicortically harvested when the modified Harrington sacral bar cannot be used (Fig. 13). Use of the Jackson technique requires knowledge
of the surgeon's ABCs: A = the axis goes to the rigid implant or rods, B = balance is brought over the center of gravity, C = the rods are contoured
to translate the axis by moving the implants over the hips.
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FIGURE 14. The Kostuik modification of the Harrington sacral bar provides a mechanical advantage. The
lever to counteract screw pullout is offset posteriorly from the center of gravity (cg) with this method. |
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Tle Kostuik modification of the Harrington sacral bar, which provides bilateral iliac crest purchase, together with sacral
connectors, increases the forward lever arm to successfully counter cantilever forces in the osteoporotic sacrum (Figs. 14 and 15).
Other techniques that are not used as often include the Dunn
McCarthy-Galveston screwrod technique and the modified Galveston-S1 technique with a 40-mm screw plus a 60-mm iliac screw.69
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FIGURE 15. Preoperative radiographs shows an alternative to anterior column support with titanium cages and compression
lag screws. Structural femoral ring allograft is stuffed with autogenous bone graft (black arrow) and fixed using 3.5-mm cancellous lag screws with washers. The screw placement allows physiologic
compression, and the washers buttress the bone graft and prevent displacement. The Kostuik modification of the Harrington sacral bar (white arrow) with dominoed connectors was used to provide an off-set
mechanical advantage to screw pullout. The L5 screws resist rotation. |
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FIGURE 16A-D. A and B, preoperative radiographs from a 69-year-old . woman with prior D and L4 laminectomies who was left
with severe pain from gross instability after decompression for spinal stenosis. The postlarninectomy instability resulted in further spinal stenosis. Gross multiplane imbalance is evident. C and D, MRI
confirms spinal stenosis due to disc bulging and interspace narrowing, with resultant ligamentous laxity and shortening hypertrophy.of the posterior longitudinal ligament and ligamentum flavus (arrows).
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FIGURE 16E-I. E and F, preoperative spot radiographs substantiate the coronal instability and sagittal flat back
deformity. G-1, postoperative correction following a stage one L2-S I anterior interbody fusion and a second-stage L2-S I posterior fusion with polyaxtal screw instrumentation. Anteriorly, the allowgraft
(arrow in G) was held by two cancellous lag screws to secure L5 to the sacrum while morselized autograft was placed in the center and resected disc spaces. Posteriorly, the polyaxial screws were used to
translate L3 to the right while the rods were engaged. The patient's pain was alleviated and independence restored. |
Assessment of postoperative fusion mass is difficult, and a new paintut detormity should alert the surgeon to anterior column failure
with posterior fusion mass fatigue despite solid fusion. Although fusion mass stress fractures may occur, they must be differentiated from plate pseudarthrosis, which occurs parallel with the sagittal axis
and may be missed on hardware removal and exploration. Stress fractures are particularly common in fusions for ankylosing spondylitis. Although exuberant bone is formed, the fusion is
osteoporotic and regularly fails. Correction requires anterior column reconstruction in addition to posterior fixation and geometric realignment. The process and principles are the same.
DISCUSSION
Osteoporosis and stenosis occur together. Both occur after disc degeneration shortens the column and causes ligamentous laxity, facet hypertrophy, and instability. A clear clinical pattern of
degeneration emerges that is consistent with the biomechanical studies of Haher et al.15 which show, as with other joints in the body, that abnormal stresses may lead to osteoarthritis. Facet arthrosis
and degeneration never occur without the presence of adjacent disc degeneration. The adjacent intact discs protect the facets from severe loading and degeneration. The anterior annulus and the
anterior longitudinal ligament are the principal support structures in extension; they protect the facets from severe loading and degeneration.
In addition to these age-related changes in overall bone volume and
shape, the most important change is the increase in percentage mineralization that occurs with increasing age. The higher percentage of mineralization increases bone stiffness, but it considerably
reduces bone's ability to absorb energy under conditions of impact loading.6,9 The architectural changes are more pronounced than the loss of bone mass. Fractures occur centrally and are initiated from
the vertebral centrum. The flattened collapsed vertebra is wider than usual and causes further stenosis. The tissue not only is compressed in the direction of the applied load, but also expands in
the transverse direction; this is known as Poisson's ratio effect.27
When decompression for stenosis is performed, the peripheral rim support is removed. Without fusion, regrowth of the posterior arch
occurs. Posterior element regrowth increases vertebral stability but further narrows the nerve root canals and the central canal. Central canal narrowing is mainly caused by the posterior facet joints, whose
regrowth reproduces the neurocompression present before surgery.17 Fusion eliminates, while instability produces, vertebral canal narrowing and spinal stenosis. Decompression for spinal stenosis
should therefore be combined with fusion, especially with degenerative spondylolisthesis. Osteoporotic patients who undergo decompression of two or more levels should also be fused because
little remaining reserve bone is available to redistribute to the periphery. Such patients are susceptible to further instability following decompression than nonosteoporotic patients, particularly if any
preexistent deformity exists (Fig. 16).
CONCLUSION
Initial spinal instability is caused by the degeneration of the intervertebral disc. The spine attempts to stabilize itself by removing
bone from its vascular vertebral center and placing it on its periphery. Age modeling of bone is toward some optimized structure at the expense of the neural contents. Bone does the best it can with the
materials and the biology it has to work with. The simultaneous findings of stenosis and osteoporosis after disc degeneration in the aging spine reflect instability phenomena that bone encounters. The
human spine is not necessarily a structure that is optimized by evolution.
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