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骨质疏松性椎体骨折

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Updated Sep 2026
Illustration: spine

本页面由机器翻译，尚未经临床医生审核。英文版本为权威版本。

您的感受

骨质疏松性骨折是指脊柱中的椎骨变得如此纤细和脆弱，以至于在日常负荷下发生裂纹。疼痛通常位于背部中央，或中背部与下背部交界处。它往往突然发作，有时甚至由弯腰、提重物或轻微绊倒等小事引发。

疼痛起初通常是尖锐的，随后转为钝痛。站立或行走一段时间、扭转身体或向前弯腰时，疼痛往往会加剧。从躺卧状态坐起可能很困难，疼痛常在醒来后或久站后加重。平躺可能会缓解疼痛。给脊柱带来负荷的日常任务会变得困难：提购物袋、从低矮的椅子上起身、整理床铺或爬楼梯。

如果骨折影响椎骨的下部，有时可能会刺激沿腿部延伸的神经。这可能导致该侧腿部的疼痛、刺痛或麻木。有些人还会拉伤包裹下背部肌肉的强韧组织层，这会增加疼痛感。

这些骨折可能影响多个椎骨，且在普通X光片上容易被漏诊。如果您超过60岁且出现突发背痛，值得进行适当的检查。骨折也意味着您的骨骼比应有的状态更脆弱，因此在未来几年内再次发生骨折（包括髋部骨折）的可能性是真实存在的。如果您已经发生过不止一次脊柱骨折，这种风险会再次升高。

大多数此类骨折会随时间自行愈合，无需手术。如果尽管使用了止痛药，您的疼痛仍然严重，有一些手术可以帮助缓解，我们将在接下来的章节中介绍。

实际发生了什么

您的脊柱是由一系列称为椎骨的骨骼堆叠而成的，每一块椎骨的前方都有一个实心的骨块来承受您的体重。健康的骨骼是一个活的支架，随着旧骨被移除和新骨被沉积而不断重建。在骨质疏松症中，这种平衡被打破：骨吸收的速度快于骨形成的速度，因此支架变得薄而多孔，就像孔洞越来越大的蜂窝一样。

每块椎骨前方的骨块被设计用来承受身体的压缩负荷，有点像一块砖承受其上方墙壁的重量。当这块“砖”变得多孔时，日常负荷（如弯腰或提重物）可能会将其压碎。骨骼被压缩并呈楔形，导致椎骨前方高度降低，脊柱在该水平处轻微前弯。这种压碎就是您所感受到的骨折，疼痛来自骨骼本身的裂纹以及它对周围组织造成的牵拉。

这些骨折最常发生在您的中背部与下背部交界处，因为该交界处承受了脊柱中更多的弯曲力。如果多块椎骨被压碎，前弯可能会累积，这会改变整个脊柱的负荷分布方式，并可能加剧您感受到的酸痛和僵硬。骨骼通常在数周到数月内自行愈合，但由于骨骼较薄，愈合后的椎骨可能会继续缓慢压缩，而相同的薄弱性意味着其他部位发生骨折的可能性依然存在。

只有大约三分之一的脊柱骨折患者会实际感受到疼痛，这就是为什么它们容易被忽视的原因。大多数情况仅通过时间和止痛药即可缓解。如果尽管采取了这些措施，您的疼痛仍然严重，则存在可以稳定压碎骨骼并缓解疼痛的手术程序，我们将在下文介绍。

我们如何处理

大多数此类骨折无需手术即可愈合。第一步是保持活动。温和的运动和活动有助于骨骼愈合，阻止进一步的骨量流失，并让您能够继续从事喜爱的活动。物理治疗对此进行指导：其目标是在骨折稳定期间重建您的力量和信心。请给予数周至数月的时间，因为骨骼通常在此期间自行愈合。在愈合过程中，可能会使用支具来支撑您的背部。止痛药物有助于您在此期间保持活动。

与此同时，我们也会关注骨骼本身。骨质疏松药物可以增强骨骼强度，并降低再次骨折的风险。维生素 D 缺乏在这些骨折中很常见，我们会在手术前进行检查并予以纠正。这项骨骼健康工作至关重要：它能改善愈合，减少并发症，并降低新发骨折的风险。这往往被忽视，但它是任何由骨质疏松引起的骨折后康复的重要组成部分。

如果经过非手术治疗试验后，您的疼痛仍然严重，我们可能会讨论一种称为椎体增强的手术。这是一种微创手术，通过骨水泥来稳定被压碎的椎体。有两种形式。椎体成形术（Vertebroplasty）直接注射骨水泥。球囊后凸成形术（Kyphoplasty）首先使用一个小球囊抬起塌陷的骨骼，然后用骨水泥填充空间，这还可以改善由骨折引起的前屈畸形。当非手术治疗效果不佳时，球囊后凸成形术是我们偏好的选择。这些手术通过小切口而非大切口进行，从而降低了老年患者的风险。在手术过程中，骨水泥有时会从骨骼中渗漏，这种情况在椎体成形术中更为常见，因此我们采用针对您骨折情况定制的技术来预防这种情况。该手术有专门的页面，其中解释了手术当天的流程以及康复过程。

预期情况

对于大多数人而言，随着骨骼自行愈合，这类骨折引起的疼痛会在数周至数月内逐渐消退。尖锐的疼痛通常先缓解，而钝痛消退得较慢。在此期间保持活动并维持肌力会有所帮助，而长时间休息反而可能因进一步削弱骨骼并增加跌倒和新伤的风险而对您不利。

如果疼痛得到良好控制，您可以预期随着骨折稳定而恢复正常活动。如果疼痛剧烈且止痛药无法缓解，进行固定骨骼的手术可以缓解该疼痛，且与单纯药物治疗相比，其益处可持续至术后第一年。这些手术还旨在支撑塌陷的椎体，以防止脊柱在该节段持续向前弯曲。

需要了解一些客观的局限性。由于您的骨骼较薄，之后在其他椎体发生新骨折是可能的，如果您年龄较大、既往有骨折史或骨密度低，风险会更高。当骨质疏松本身在骨折护理的同时通过药物治疗时，风险会降低。有些人还会发现塌陷的椎体随时间推移进一步失去高度，这是疏松骨骼的特性表现，而非治疗失败的迹象。

如果骨折未予处理且前屈逐渐加重，尤其是存在多处骨折时，这种形态改变会影响脊柱的负荷传递并持续引发问题。关注骨骼健康、保持活动并坚持完成骨质疏松治疗，能让您获得最佳愈合机会并保持行动自如。

何时就医

如果您超过60岁，即使仅因轻微绊倒或简单弯腰便出现突发背痛，请尽快就诊全科医生。此类骨折在普通X光片上极易漏诊，因此请询问是否需要进一步影像学检查。若出现腿部新的无力、麻木或刺痛感，或出现膀胱或肠道控制障碍，请前往急诊科。若经过数周药物治疗后疼痛仍持续剧烈，或您已发生过此类骨折且疼痛复发或转移至其他节段，或您已知存在骨质疏松且出现任何新的背痛，请要求专科医生评估。

Reviewed by AI synthesis (v2) — pending human review · 9 September 2026.

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Evidence & references

This is the clinical evidence summary written for health professionals. It is technical, and it lists the research this page was built from. You do not need to read it to understand your treatment or to make a decision about it.

Anatomy & Pathophysiology

Vertebral Column Anatomy

  • The vertebral column comprises 33 vertebrae divided into five sections: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal [16].
  • The sacral and coccygeal vertebrae are fused, typically allowing for 24 mobile segments [16].
  • A typical vertebra comprises an anterior body and a posterior arch that enclose the vertebral canal [16].
  • The neural arch is composed of two pedicles laterally and two laminae posteriorly that are united to form the spinous process [16].
  • To either side of the arch of the vertebral body is a transverse process and superior and inferior articular processes [16].
  • The articular processes articulate with adjacent vertebrae to form synovial joints [16].
  • The relative orientation of the articular processes accounts for the degree of flexion, extension, or rotation possible in each segment of the vertebral column [16].
  • The spinous and transverse processes serve as levers for the numerous muscles attached to them [16].
  • The length of the vertebral column averages 72 cm in men and 7 to 10 cm less in women [16].
  • The vertebral canal extends throughout the length of the column and provides protection for the spinal cord, conus medullaris, and cauda equina [16].

Intervertebral Disk Anatomy

  • The intervertebral disk connects adjacent vertebral bodies [6].
  • The adjacent vertebral bodies, the disk, and the facet joints constitute the functional spinal unit that provides mechanical stability and allows physiologic motion [6].
  • The intervertebral disks run between vertebral bodies from C2 to S1 and function to resist loads on the spine and provide stability [18].
  • The disks contribute up to one-third of the height of the spinal column [18].
  • The disk consists of the cartilaginous end plates of the vertebral bodies, the outer anulus fibrosus, and the inner nucleus pulposus [18].
  • The end plate serves as a point of attachment of the disk to the superior and inferior surfaces of the vertebral bodies [18].
  • The end plate is a thin layer of hyaline cartilage [18].
  • The nucleus pulposus is centrally located and confined by the end plates and the anulus fibrosus [6].
  • The nucleus pulposus resists compressive loads, dampens mechanical loads, and evenly distributes forces onto the end plates [6].
  • The nucleus pulposus is the remnant of the embryonic notochord and comprises the gelatinous center of the intervertebral disk [18].
  • The extracellular matrix of the nucleus pulposus is composed primarily of type II collagen and aggrecan, which makes it relatively hydrophilic [18].
  • The nucleus pulposus serves to resist axial loads as well as provide height to the intervertebral disk [18].
  • The anulus fibrosus is peripheral to the nucleus pulposus and confines the nucleus pulposus [6].
  • The anulus fibrosus is designed to resist tensile loads, allow spinal motion, provide mechanical connection between the vertebrae, and confine the nucleus pulposus [6].
  • The anulus fibrosus consists of concentrically layered fibrous cartilage lamellae primarily composed of type I collagen [18].
  • The fibers of the anulus fibrosus run in alternating oblique trajectories [18].
  • The anulus fibrosus resists tensile forces within the spine, including those due to the compression of the nucleus pulposus [18].
  • The end plates form the interface between the vertebrae and the disk and define the upper and lower boundaries of the disk [21].
  • The central portion of the end plate provides a major pathway for nutrients from the vertebral bodies to diffuse into the disk [21].

Disk Physiology and Pathophysiology

  • In a normal healthy lumbar disk, large aggregating proteoglycans (aggrecan and versican) constitute a high percentage of the dry weight in the nucleus [21].
  • Glycosaminoglycan molecules (keratan sulfate and chondroitin sulfate) decorate the aggrecan and versican core protein and are highly negatively charged [21].
  • The highly negatively charged glycosaminoglycans create a highly hydrophilic matrix that attracts H2O molecules [21].
  • The attraction of H2O molecules provides swelling pressure that counteracts the axial loads encountered by the disk [21].
  • The matrix is viscoelastic and therefore dissipates mechanical energy and is subject to creep [21].
  • Disk height is less at the end of each day due to creep [21].
  • The adult intervertebral disk is avascular and derives its nutrition through diffusion from terminal capillaries in the vertebral bodies just below the end plates [18].
  • In the adult, the blood supply ends at the bony end plate of the vertebral body and the outer anulus fibrosus [21].
  • Most of the disk is considered immunologically isolated due to its avascularity [21].
  • Nutrients are supplied to the disk cells primarily through diffusion [21].
  • As the disk gets larger during development, the distances that nutrition must diffuse across become larger, further impeding nutritional supply to the disk cells [21].
  • The decrease in nutritional transport is thought to contribute to disk degeneration [21].
  • Innervation of the intervertebral disk is confined to the peripheral anulus fibrosus [21].
  • The sinuvertebral nerve, which arises from the dorsal root ganglion, innervates the outer anulus fibrosus [21].
  • In some degenerated disks with fissures, nerve fibers may be found deeper in the anulus fibrosus [21].
  • The normal nucleus pulposus is not innervated [21].
  • Pain sensation from the disk arises only from the anulus fibrosus [21].
  • The nucleus pulposus can generate molecules such as cytokines and proteinases that can lead to pain [21].
  • With normal ageing, glycosaminoglycan production diminishes, leading to gradual desiccation of the disc [19].
  • The annulus fibrosus develops fissures and disc nuclear material may prolapse through during degeneration [19].
  • The discs lose height and bulge beyond the margins of the vertebral bodies during degeneration [19].
  • Disc protrusion against the ligaments causes formation of marginal osteophytes [19].
  • Adjacent vertebral end plates ossify and become sclerotic while fatty change occurs in the subchondral bone marrow during spondylosis [19].
  • Disc degeneration results in altered biomechanics and increased loading forces on the facet joints [19].
  • Facet joint osteoarthritis may lead to osteophyte encroachment into the canal causing spinal lateral recess stenosis [19].
  • The ligamentum flavum thickens, which contributes to stenosis, while the disc bulges from anteriorly into the spinal canal [19].

Osteoporosis Pathophysiology

  • Osteoporosis is the most common metabolic bone disease resulting from imbalance between bone formation and bone resorption [2].
  • Spinal fractures are the most common manifestation of osteoporosis [2].
  • Only one in three patients with spinal fractures are symptomatic [2].
  • In elderly patients, osteoporosis-related spinal fractures have similar morbidity and mortality as hip fractures [2].
  • Osteoporosis and low bone mass are present in about 50% of elective spine patients older than 50 years [2].
  • Osteoporosis and low bone mass negatively affect clinical outcomes and are associated with increased complications and revision surgery [2].
  • Vitamin D deficiency is present in the majority of spine patients [2].

Clinical Presentation

  • A history of fragility fracture significantly increases the risk of another fracture [15].
  • The relative risk of a subsequent fracture is two to three times higher in women with a prior fragility fracture [15].
  • The relative risk of a subsequent fracture is up to six times higher in men with a prior fragility fracture [15].
  • A history of greater than a single vertebral fracture significantly increases the risk of further vertebral fractures [15].
  • In a meta-analysis of nontreated patients enrolled in vertebroplasty studies, 18% had a secondary fracture within 12 months [15].

Investigations

Imaging Modalities

  • Dual energy x-ray absorptiometry (DXA) is the benchmark to assess bone mineral density (BMD) [25].
  • DXA measures areal BMD in g/cm² of the proximal femur, lumbar spine, and distal radius [25].
  • DXA is accurate and precise when calibrated and performed properly [25].
  • DXA involves a very low radiation dose [25].
  • BMD is reported as a standard deviation difference to a reference standard [25].
  • T-score is the reference standard for young healthy females [25].
  • Z-score is the reference standard for age- and gender-matched subjects [25].
  • Vertebral fracture assessment (VFA) can be performed at the time of DXA [25].
  • VFA identifies occult vertebral fracture in 20% to 30% of cases [25].
  • VFA is useful to change a diagnosis from low bone mass (osteopenia) to osteoporosis [25].
  • Opportunistic CT uses CT data to estimate bone status [25].
  • CT is based on the attenuation coefficient called the Hounsfield unit (HU) [25].
  • Hounsfield units are related to BMD and can be used to estimate BMD and the presence of osteoporosis [25].
  • PACS tools can calculate mean HU for any elliptical region of interest [25].
  • Most osteoporotic vertebral fractures can be diagnosed by plain radiographs or CT [26].
  • MRI can show edema in the vertebral body to indicate a recent fracture when age determination is required [26].
  • An acute measured height change of greater than 1 inch is suggestive of an acute vertebral fracture [26].

Laboratory and Preoperative Assessment

  • Greater than 75% of patients older than 50 years having elective spine surgery have vitamin D insufficiency or deficiency [14].
  • Vitamin D deficiency is linked to increased pain severity in spinal stenosis [14].
  • Ravindra demonstrated slower fusion and lower rates of success in vitamin D–deficient patients [14].
  • Kim found that baseline low vitamin D was associated with worse Oswestry Disability scores at follow-up [14].
  • Vitamin D deficiency is treatable but takes 6 weeks [14].
  • Osteoporosis is linked to subsidence of cages, pedicle screw loosening, proximal junction failure, poorer fusion rates, increased spondylolisthesis after laminectomy, and higher rates of revision surgery [14].
  • Bjerke reviewed 140 lumbar fusion patients and found that 10 were osteoporotic and 59% had low bone mass [14].
  • Nonunion was 50% in osteoporotic patients compared with 18% in those with low bone mass or normal BMD [14].
  • Osteoporosis-related complications occurred in 23% of patients with normal BMD, 28% of patients with low bone mass, and 46% of osteoporotic patients [14].
  • Complication rates worsened relative to BMD when more than single-level fusion was performed [14].
  • The AOA suggests using the same principles as outlined for secondary fracture prevention for preoperative bone health optimization [14].
  • Inclusion criteria for preoperative bone health optimization assessment include all patients having thoracolumbar surgery who are older than 50 years [14].
  • Preoperative patients are recommended to consume vitamin D3 2,000 U daily and 1,200 mg calcium in the diet [14].
  • Preoperative patients should be assessed for fall risk and considered for physical therapy if warranted [14].
  • Patients who do not need DXA or who screen negative for DXA should undergo surgery [14].
  • Patients with low bone mass or osteoporosis should be considered for preoperative bone health optimization [14].
  • If medically indicated, patients are treated with diphosphonate or anabolic medication before surgery [14].
  • The duration of preoperative treatment is unknown, but effects of bone strength and physiology are seen within 2 months [14].
  • A minimum of 3 months of preoperative treatment is recommended if clinically possible before surgery [14].
  • Longer treatment up to 9 months should be considered for multilevel or high-risk cases such as osteotomy [14].
  • Antiosteoporosis medications should be continued postoperatively [14].
  • Multiple RCTs comparing biphosphonates and placebo in patients undergoing lumbar spine fusion show improved clinical outcomes, radiologic outcomes, and lower risk of complications [14].
  • Biphosphonates do not appear to be associated with any impairment of bone health [14].
  • One RCT and multiple cohort studies show that teriparatide can lead to improved clinical outcomes, radiologic outcomes, and lower risk of complications in spinal fusion patients [14].

Treatment

Non-Operative Management

  • The initial treatment of osteoporotic vertebral fractures is nonsurgical [2].
  • Secondary fracture prevention is performed in less than 20% of cases following osteoporosis-related fractures [2].
  • Secondary fracture prevention includes education, assessment of bone health, nutritional supplements, weight-bearing exercise, fall prevention, and pharmaceutical medications if indicated [2].
  • A history of fragility fracture increases the relative risk of another fracture by two to three times in women and up to six times in men [15].
  • Secondary treatment was given in 10% of patients in a Medicare database analysis but was associated with a reduced risk of fracture by 40% [15].
  • The American Orthopaedic Association (AOA) Own the Bone program is located in all states and 150 sites in the United States [15].
  • The AOA Own the Bone program significantly improves compliance with treatment recommendations after fragility fracture [15].
  • A prospective randomized controlled non-inferiority trial found that rigid brace, soft brace, and no brace treatments for osteoporotic compression fractures without neurologic injury had comparable outcomes [1].
  • Vitamin D deficiency is present in the majority of spine patients and should be corrected after fracture and before elective surgery [2].
  • Routine use of vitamin D (1,000 to 2,000 IU/day) and calcium supplementation for all spine fusion patients aged 65 years or older may help avoid nonunion and infection [28].
  • Target serum 25-hydroxyvitamin D levels are 30 ng/mL [28].

Operative Management: Cement Augmentation

  • Vertebroplasty or kyphoplasty is considered for osteoporotic vertebral fracture in patients who are hospitalized for pain, those who do not improve with nonoperative care, or those who have progressive collapse [2].
  • A 2009 multicenter trial by Kallmes et al. found that vertebroplasty and a simulated procedure without cement resulted in similar improvements in pain [29].
  • A 2009 multicenter, randomized, double-blinded placebo-controlled trial by Buchbinder et al. identified no clinical benefit to vertebroplasty compared to a simulated procedure at follow-up visits ranging from 1 week to 6 months [29].
  • A multicenter European randomized control trial by Klazen et al. concluded that vertebroplasty was safe and provided immediate and sustained pain relief and improvement in quality of life to a significantly greater degree than nonsurgical treatment [29].
  • A randomized control study by Boonen et al. showed that kyphoplasty and vertebroplasty significantly reduced pain, improved early mobility, and enhanced short-term quality of life compared to noninvasive management options [29].
  • A systematic review by Taylor et al. showed that kyphoplasty and vertebroplasty significantly reduced pain, improved early mobility, and enhanced short-term quality of life compared to noninvasive management options [29].
  • Balloon kyphoplasty may correct the loss of vertebral body height, a predictor of progressive kyphosis, but this has only been confirmed on a limited basis for kyphoplasty and not for vertebroplasty [29].
  • Vertebroplasty and kyphoplasty are largely equivalent in their ability to provide pain relief and functional improvement, with little advantage gained by performing kyphoplasty given its significantly greater cost [29].
  • A Medicare database analysis by Edidin et al. identified lower mortality (39% vs. 50%) in patients treated with vertebroplasty compared to patients treated noninvasively [29].
  • A 2018 Cochrane Review by Buchbinder et al. analyzing 21 randomized and quasi-randomized controlled trials concluded that current high- to moderate-quality evidence does not support a role for vertebroplasty in the routine treatment of acute or subacute osteoporotic vertebral fractures [29].
  • The 2018 Cochrane Review by Buchbinder et al. could not identify sufficient evidence to support any clinically relevant benefit to vertebroplasty compared to placebo [29].
  • Subgroup analyses in the 2018 Cochrane Review showed that results were not affected by whether the duration of pain was less than or greater than 6 weeks [29].
  • Adverse events identified in the 2018 Cochrane Review included thromboembolic events, cement leakage, spinal cord compression, neurologic injury, respiratory failure, and osteomyelitis [29].
  • A randomized study by Firanescu et al. comparing vertebroplasty with a placebo (simulated procedure) control group found a similar, statistically significant reduction in pain as measured by visual analog scale (VAS) scores for both groups during 12-month follow-up [29].

Preoperative Bone Health Optimization

  • Greater than 50% of patients older than 50 years having elective spine surgery have low bone mass or osteoporosis [14].
  • Vitamin D deficiency is treatable but will take 6 weeks [14].
  • In a review of 140 lumbar fusion patients by Bjerke, nonunion was 50% in osteoporotic patients compared with 18% in those with low bone mass or normal BMD [14].
  • In a review of 140 lumbar fusion patients by Bjerke, osteoporosis-related complications occurred in 23% of patients with normal BMD, 28% in patients with low bone mass, and 46% in osteoporotic patients [14].
  • Inclusion criteria for preoperative bone health optimization include all patients having thoracolumbar surgery who are older than 50 years of age [14].
  • Preoperative patients are recommended to consume vitamin D3 2,000 U daily and 1,200 mg calcium in diet [14].
  • Preoperative patients should be assessed for fall risk and consider physical therapy if warranted [14].
  • Patients who have low bone mass or osteoporosis should be considered for preoperative bone health optimization [14].
  • The author recommends a minimum of 3 months of preoperative treatment if clinically possible, as effects of bone strength and physiology are seen within 2 months [14].
  • For multilevel or high-risk cases such as osteotomy, longer treatment up to 9 months should be considered [14].

Complications

  • Osteoporosis and vitamin D deficiency are associated with poorer outcomes, recurrent fractures, and higher complication risks [2].
  • Osteoporosis and low bone mass negatively affect clinical outcomes and are associated with increased complications and revision surgery in elective spine patients older than 50 years [2].
  • Preoperative and postoperative treatment of osteoporosis in spine surgery patients has been shown to improve outcomes and reduce complications [2].

References

[1] Aaos Comprehensive Orthopaedic Review 3. Assessment and Treatment of Osteoporosis and Vertebral Fractures* > XV. Conclusion > Bibliography.

[2] Aaos Comprehensive Orthopaedic Review 3. Assessment and Treatment of Osteoporosis and Vertebral Fractures* > XV. Conclusion.

[6] Aaos Comprehensive Orthopaedic Review 3. Intervertebral Disk > I. Function.

[14] Aaos Comprehensive Orthopaedic Review 3. Assessment and Treatment of Osteoporosis and Vertebral Fractures* > XIV. Preoperative Bone Health Optimization.

[15] Aaos Comprehensive Orthopaedic Review 3. Assessment and Treatment of Osteoporosis and Vertebral Fractures* > XII. Secondary Fracture Prevention.

[16] Campbell S Operative Orthopaedics 4 Volume Set. RECONSTRUCTION OF THE PATELLOFEMORAL AND PATELLOTIBIAL LIGAMENTS WITH A SEMITENDINOSUS TENDON GRAFT > ANATOMY OF VERTEBRAL COLUMN.

[18] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Spinal Anatomy > Intervertebral Disk.

[19] Apley And Solomon S Concise System Of Orthopaedics And Trauma. INTERVERTEBRAL DISC LESIONS.

[21] Aaos Comprehensive Orthopaedic Review 3. Intervertebral Disk > II. Anatomy.

[25] Aaos Comprehensive Orthopaedic Review 3. Assessment and Treatment of Osteoporosis and Vertebral Fractures* > V. Diagnosis of Osteoporosis.

[26] Aaos Comprehensive Orthopaedic Review 3. Assessment and Treatment of Osteoporosis and Vertebral Fractures* > XIII. Osteoporotic Vertebral Fractures.

[28] Rockwood And Green S Fractures In Adults. Imaging of Cervical Spine Fractures and Dislocations > Special Considerations in Thoracolumbar Spine Fractures and Dislocations > Treatment Options for Osteoporotic Vertebral Fractures.

[29] Rockwood And Green S Fractures In Adults. Imaging of Cervical Spine Fractures and Dislocations > Operative Treatment of Osteoporotic Vertebral Fractures > Cement Augmentation.

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