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52 Post-Infectious Deformity
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a
b
Fig. 52.2 (a and b) Show CT and MRI imaging revealing a L1 vertebral body collapse and
kyphotic deformity. It can be classied as Kyphosis Classication (Rajasekaran) type IIIB
(Appendix P) [Courtesy of Prof. Alpaslan Şenköylü]
52.9 What Should Patient andFamily Know?
Postinfectious kyphosis may present with pain, deformity and neurological decit
(mild to complete). Treatment will depend on the amount of pain, reduction in activities of daily living, degree of deformity (kyphosis), patients’ comorbidities and
patients’ aspirations. Surgical intervention can carry its own risk of complications
including paralysis, rod breakages and a higher risk of infection. While the surgical
team will optimise patients preoperatively and plan accordingly, patient factors also
play a major role in the recovery process. A patient with multiple comorbidities and
poor immune status will not do well with major surgical intervention. Each patient
needs to be assessed independently prior to any surgical intervention.
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S. Haleem
a
b
Fig. 52.3 (a and b) Show satisfactory coronal and sagittal alignment after posterior vertebral
column resection [Courtesy of Prof. Alpaslan Şenköylü]
Further Readings
Boachie-Adjei O, etal. Late treatment of tuberculosis-associated kyphosis: literature review and
experience from a SRS-GOP site. Eur Spine J. 2013;22 Suppl 4(Suppl 4):641–6.
Lonstein JE, etal. Neurologic decits secondary to spinal deformity. A review of the literature and
report of 43 cases. Spine (Phila Pa 1976). 1980;5(4):331–55.
Rajasekaran S, etal. A classication for kyphosis based on column deciency, curve magnitude,
and osteotomy requirement. J Bone Joint Surg Am. 2018;100(13):1147–56.
Paget’s Disease
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YannPhilippeCharles
53.1 Definition
Paget’s disease, also known as osteitis deformans, represents a metabolic bone disorder. The spine represents the second most commonly affected part of the skeleton
after the pelvis. Monostotic and polyostotic patterns exist. Paget’s disease is usually
diagnosed after the age of 50 years, and the overall prevalence is reported around
2% to 3%, although ethnic differences have been described. The prevalence
increases in elderly patients. The etiology and exact pathophysiology remain
unclear. On the one hand, viral infections (paramyxovirus, syncytial respiratory
virus) have been incriminated. On the other hand, different genetic mutations
(sequestosome) might play a role.
53.2 Natural History
The pathophysiology of Paget’s disease is characterized by dysregulation between
osteoblastic and osteoclastic activity. Three main phases of the disease exist when
the spine is involved. The rst phase represents the initial osteolytic phase which is
represented by mainly osteoclastic activity. The second phase is characterized by a
combination of osteoblastic and osteoclastic activities. The third phase represents
Supplementary Information The online version contains supplementary material available at
[https://doi.org/10.1007/978- 3- 030- 80356- 8_53].
Y. P. Charles (*)
Service de Chirurgie du Rachis, Hôpitaux Universitaires de Strasbourg, Faculté de Médecine,
Maïeutique et Sciences pour la Santé, Université de Strasbourg, Strasbourg, France
e-mail: YannPhilippe.CHARLES@chru-strasbourg.fr
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
A. Şenköylü, F. Canavese (eds.), Essentials of Spine Surgery,
https://doi.org/10.1007/978-3-030-80356-8_53
321
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the last stage which is characterized by new bone formation. An additional inactive
late stage has further been described as sclerotic phase, where stimulation of new
osteoblasts and osteoclasts ceases. During this late stage, the bone is metabolically
inactive, but it maintains a sclerotic coarsened architecture.
Y. P. Charles
53.3 Physical Examination
Clinical symptoms of Paget’s disease depend on the localization of the skeleton and
the stage of the disease. However, patients can be asymptomatic, and pathologic
ndings may be discovered incidentally on imaging or blood tests. In patients with
spinal involvement, back pain represents the most common symptom (Chap. 41).
The spinal level is determined by palpation, and pain intensity is assessed on a
visual analog scale (VAS 1-10).
In some cases, excessive bone formation can lead to narrowing of the spinal
canal. In the thoracic spine, this might lead to slowly progressive spinal cord compression and paraparesis. In the lumbar spine, spinal canal narrowing can lead to
radicular pain and neurogenic claudication. Physical examination should include
neurologic radicular sensory and motor testing (Videos 53.4 and 53.9). The sensory
examination should investigate paresthesia, and a pinprick test should be performed.
The motor examination requires muscle strength testing according to the Medical
Research Council scale from 1 to 5. If spinal cord compression is suspected, pyramidal tract signs such as hyperreexia and positive Babinski sign should be
investigated.
Blood Tests. Alkaline phosphatase (ALP) is typically elevated at stages with
increased bone metabolism. This biomarker correlates with the active bone resorption and formation by osteoclasts and osteoblasts. It is therefore used for follow-up
in patients that are treated with bisphosphonates. Hepatic enzymes should be
checked in parallel, since ALP might also increase in diseases of the liver.
Osteocalcin is secreted solely by osteoblasts. This protein hormone has no diagnostic value in patients with Paget’s disease.
53.4 Imaging
The standard radiographic examination consists of anteroposterior (AP) and lateral
radiographs of the spine. Radiographic ndings depend on the stage of the disease.
During the initial phase, osteolysis can be present at the level of the vertebral body.
During the course of the disease, periosteal and endosteal bone apposition will
result in characteristic sclerotic lines parallel to the end plates (Fig.53.1). Finally,
cortical thickening will result in a framed picture and an enlargement of the vertebral body in the sagittal and coronal planes.
Computed tomography (CT) scan provides good-quality images of bony lesions.
In the initial phase, osteoclastic activity will result in osteolytic images (Fig.53.2).
In the second phase, periosteal apposition and endosteal resorption can be present
53 Paget’s Disease
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Fig. 53.1 Radiographs showing periosteal and endosteal bone apposition parallel to the end
plates of L4
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Fig. 53.2 Sagittal and axial CT demonstrating osteolytic images of the L2 vertebral body and
posterior elements during the initial phase
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Y. P. Charles
Fig. 53.3 Sagittal and axial CT images showing periosteal apposition and endosteal resorption at
L1 during the second phase of Paget’s disease
simultaneously (Fig. 53.3). In the third phase, sclerotic bone formation can be
observed, also described as dense “ivory vertebra” (Fig.53.4).
Magnetic resonance imaging (MRI) is indicated to evaluate the spinal cord or
cauda equina if spinal stenosis is present. The coarsened aspect of the vertebra can
be observed on T1-weighted images (Fig.53.5), and T2-STIR sequences might help
to identify an active spot, but CT is preferred as rst-line imaging when evaluating
osteolysis and bone formation. Bone scintigraphy using 99-technetium substrates
and SPECT can aid the diagnosis of Paget’s disease and demonstrate the distribution of different spots on the skeleton (Fig.53.6).
53.5 Differential Diagnosis
Osteolytic images can be present in osteoporotic fractures and in vertebral metastases (breast, kidney, lung cancer) (Chap. 63), aggressive hemangioma (Chap. 55),
giant cell tumor (Chap. 57), myeloma (Chap. 61), chordoma (Chap. 62), and chondrosarcoma. Differential diagnoses of dense sclerotic bone images include metastases (prostate cancer), osteosarcoma (Chap. 38), carcinoid, and Hodgkin’s lymphoma.
53 Paget’s Disease
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Fig. 53.4 Sagittal and axial CT images showing sclerotic bone formation at L4 during the third
phase of Paget’s disease
53.6 Treatment Options
The management of Paget’s disease relies on normalization of bone remodeling and
the treatment of pain. Analgesics, nonsteroidal anti-inammatory drugs, and antineuropathic drugs are prescribed. Calcitonin was historically used in the treatment
of bone metabolism. Today, different bisphosphonates (etidronate, clodronate,
pamidronate, risedronate, zoledronate) were compared in clinical trials and represent the most efcient treatment. Surgical treatment is rarely indicated.
Decompression and fusion might only be considered in neurologic complications
and major osteolysis.
53.7 Expected Outcomes
Conservative treatment using bisphosphonates usually stabilizes bone remodeling
and improves the quality of life for the patient. Clinical and radiologic follow-up is
mandatory since complications might develop.
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Fig. 53.5 T1-weighted
sagittal MRI demonstrating
the coarsened structure of
the vertebral body at L1
Y. P. Charles
53.8 Potential Complications
Bone is structurally weak in the osteolytic phase, and vertebral compression fractures can occur. Neurologic complications might appear in severe spinal canal stenosis due to excessive bone apposition. Neoplastic transformation is very rare in the
spine (0.7%) and represents only 7% of all sarcomatous degeneration in Paget’s
disease.
53.9 What Should Patient andFamily Know?
Paget’s disease is mostly asymptomatic, but pain and neurologic symptoms can
occur, usually after the age of 50 to 60 years. The entire skeleton needs to be initially checked using scintigraphy. Bisphosphonates represent the main antiresorptive treatment of bone metabolism. ALP dosage is required for monitoring bone
metabolism.
53 Paget’s Disease
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Fig. 53.6 Bone
scintigraphy demonstrating
polyostotic Paget’s disease
with involvement of the
spine (T11) and the pelvis
327
Further Readings
Dell’Atti C, Cassar-Pullicino VN, Lalam RK, Tins BJ, Tyrell PNM.The spine in Paget’s disease.
Skelet Radiol. 2007;36:609–26.
Ralston SH.Clinical practice. Paget’s disease of bone. N Engl J Med. 2013;368(7):644–50.
Rolvien T, Butscheidt S, Zustin J, Amling M. Skeletal dissemination in Paget’s disease of the
Spine. Eur Spine J. 2018;27(Suppl 3):453–7.
Ankylosing Disorders oftheSpine:
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ASandDISH
YannPhilippeCharles
54.1 Definition
Among ankylosing spinal disorders, ankylosing spondylitis (AS) and diffuse idiopathic skeletal hyperostosis (DISH) represent two distinct etiologies. Both entities
will be presented in parallel in the following chapter, since certain aspects, such as
stiffness and the risk for unstable spinal fractures, are similar for both diseases.
AS belongs to the group of axial spondyloarthropathies, which refers to a group
of inammatory rheumatic diseases. AS, also known as Bechterew’s disease, is
characterized by chronic inammation of the joints and ligaments of the spine
which leads to pain and stiffness. Vertebrae may fuse and result in a rigid spinal
deformity such as cervical and thoracolumbar kyphosis. The prevalence of AS
ranges between 0.1% and 1.4%. AS affects males two to three times more often than
females. The onset occurs before the age of 45 years. A positive family history is
often present. A gene known as the HLA-B27 is thought to be a risk factor.
DISH, initially described by Forestier and Rotés-Querol as senile ankylosing
hyperostosis, represents a noninammatory disorder that is characterized by ossication of ligaments and joint capsules. It typically occurs in the axial skeleton where
progressive ossication of the anterior longitudinal ligament and bone formation
between vertebral bodies results in spinal ankylosis. The prevalence of DISH ranges
between 3% and 6% in the population over 40 years and increases with age. The sex
ratio between males and females is 2:1.
54
Supplementary Information The online version contains supplementary material available at
[https://doi.org/10.1007/978- 3- 030- 80356- 8_54].
Y. P. Charles (*)
Service de Chirurgie du Rachis, Hôpitaux Universitaires de Strasbourg, Faculté de Médecine,
Maïeutique et Sciences pour la Santé, Université de Strasbourg, Strasbourg, France
e-mail: YannPhilippe.CHARLES@chru-strasbourg.fr
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
A. Şenköylü, F. Canavese (eds.), Essentials of Spine Surgery,
https://doi.org/10.1007/978-3-030-80356-8_54
329
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