Cysts and Other Benign Lesions

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Chapter 2 Cysts and Other Benign Lesions

Jae-Soo Koh, Ung-Kyu Chang, Terri Haddix

1 Langerhans Cell Histiocytosis
2 Aneursymal Bone Cyst
3 Synovial Cyst
4 Fibrous Dysplasia
5 Pyogenic Osteomyelitis
6 Tuberculous Osteomyelitis
7 Extradural Arachnoid Cyst

INTRODUCTION

Langerhans cell histiocytosis (LCH) is an abnormal histiocyte proliferation producing granulomatous skeletal lesions. It has not been confirmed whether LCH is a real tumor or inflammatory process. Clinically, it is considered a malignant lesion, because it has a tendency toward local recurrence.

Aneurysmal bone cysts are benign expansile lesions characterized by small and large cavernous spaces filled with clotted-blood fluid. They may arise de novo, or they may secondarily complicate other benign and malignant bone tumors that have undergone hemorrhagic cystic change.

Spinal synovial cysts are cystic masses involving the spinal canal as a result of degenerative changes in the facet joints, trauma, metaplasia, the presence of developmental rests, or excess stress inflicted at the facet joints coupled with the herniation of synovial tissue.

Fibrous dysplasias are bony lesions characterized by the metaplastic replacement of the medullary component of one bone (monostotic), or less commonly of several bones (polyostotic), with fibrous tissue and irregular osteoid formation. This disorder involves multiple symptoms.

Infectious lesions of the vertebral body (bacterial or tuberculous) are another category that should be differentiated from the metastatic or primary bone tumors. Bacteria enter the bone marrow through vascularized subchondral bone adjacent to the endplate.

In tuberculous spondylitis, the lesion starts from the initial inoculum in the anterior vertebral body.

Spinal extradural arachnoid cysts are thought to be an extradural extension of an arachnoid membrane and cerebrospinal fluid (CSF) through a small defect in the dura. Several theories have been suggested about the pathogenesis of the lesion and the mechanism of cord compression.

LANGERHANS CELL HISTIOCYTOSIS

EPIDEMIOLOGY

• The umbrella phrase LCH is now used in lieu of the previous clinical diagnoses of eosinophilic granuloma (localized, unifocal, or multifocal bony involvement), Hand–Schüller–Christian disease (localized bone [usually skull] involvement, exophthalmos, and diabetes insipidus), and Letterer–Siwe disease (disseminated disease).
• There has been a long-standing debate whether LCH represents a true neoplasm or merely an inflammatory process.1
• LCH is often considered a disease of childhood, but in a larger series,2 approximately 40% of the study population was younger than 20 years old; overall, LCH lesions were marginally more common in females than in males.

DISTRIBUTION

• In the combined results of several studies, the involvement of the spine by LCH appears to be a unique feature of the pediatric subpopulation.3
• In this combined series, more than three-quarters of the vertebral LCH lesions were found in the cervical and thoracic segments; multiple level involvement was common.

HISTOLOGY/GRADING

• The histologic feature of LCH consists of Langerhans cells, featured with grooved nuclei and faintly eosinophilic cytoplasm, and variable amounts of inflammatory cells including eosinophils, lymphocytes, plasma cells, and neutrophils (Fig. 2-1).
• In some circumstances, eosinophils comprise a large portion of the lesion.
• Langerhans cells demonstrate immunoreactivity for S100 (Fig. 2-2) and CD1a (Fig. 2-3).
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Fig. 2-1 Langerhans cell histiocytosis. This lesion consists primarily of larger Langerhans cells with grooved nuclei and eosinophils (hematoxylin–eosin stain, ×200).

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Fig. 2-2 Langerhans cells are immunoreactive for S100 (×200).

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Fig. 2-3 Langerhans cell histiocytosis. Immunoreactivity for CD1a (×200).

RADIOLOGY

Radiography and Computed Tomography (CT)

• Lytic non-sclerotic destructive vertebral lesion.
• Enhancing soft tissue mass with or without paraspinal or epidural mass.

Magnetic Resonance Imaging (MRI)

• Low signal soft tissue mass on T1-weighted image (T1WI), heterogeneously high signal soft tissue mass on T2-weighted image (T2WI; Fig. 2-4).
• Spared disc space (Fig. 2-5).
• Homogeneous enhancement.
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Fig. 2-4 Axial MR image. Low signal infiltrative lesion is shown in the sacrum on T1WI (left), intermediate signal on T2WI (middle), and homogeneous enhancement (right). Epidural mass formation and dural sac compression are observed.

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Fig. 2-5 Same signal change is shown on the sagittal image.

ANEURSYMAL BONE CYST

EPIDEMIOLOGY

• Aneurysmal bone cysts (ABCs) are characterized by small and large cavernous spaces filled with clotted-blood fluid.
• ABC is a benign and expansile, non-neoplastic lesion that destroys the bony architecture.4
• ABC represents approximately 1% of all primary bone tumors.
• The majority of ABCs appear before the age of 20 years, and any bone segment may be affected. Males and females are evenly affected.
• Approximately 10–30% of these tumors arise from the spine. They represent approximately 15% of all primary mobile spine tumors.5

DISTRIBUTION

• The cervical, thoracic, and lumbar spines are similarly affected and in most of the reported cases, the posterior elements of the vertebrae were the site of the lesion. Hay et al6 reported a series of 12 sacral lesions out of 92 cases of ABC in the spine.
• The etiology of ABCs is obscure, although the following theory is generally accepted. The aneurysmal bone cysts may be caused by development of a vicious hemodynamic cycle in a bone that is the site of a congenital vascular anomaly. This cycle is triggered by trauma or the development of other pathology, which interferes with venous drainage of the area. As a result, subsequent venous pressure increases, and a dilated and engorged vascular bed develops in the affected bone.4
• ABC may arise de novo (primary ABC) or secondarily complicate other benign and malignant bone tumors (secondary ABC) that have undergone hemorrhagic cystic change.

HISTOLOGY

• Pathologically, ABCs contain multiple fluid-filled cavities separated by multiple fibrous septa. The new bone is commonly parallel to fibrous septa (Fig. 2-6). These large spaces filled with blood do not have an endothelial lining.7
• The fibrous septa are composed of a moderately dense cellular proliferation of bland fibroblasts, with scattered osteoclastic giant cells and reactive new bone (Fig. 2-7). In approximately one-third of cases, the bone is basophilic and has been termed “blue bone” (Fig. 2-8).
• Mitoses are commonly present and can be numerous, but atypical forms are absent.
• The majority of secondary ABCs develop in association with benign neoplasms, most commonly giant cell tumor of bone, osteoblastoma, chondroblastoma, and fibrous dysplasia.
• ABC-like change may also occur in sarcoma, particularly in telangiectatic osteosarcoma.
image

Fig. 2-6 The multi-locular cystic architecture of the lesion is evident under low-power examination. Reactive bone formation in septa is oriented along long axes (hematoxylin–eosin, ×40).

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Fig. 2-7 A few osteoclastic giant cells are seen in septa of ABC, and the number of nuclei is not so numerous as in giant cell tumor (hematoxylin–eosin stain, ×100).

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Fig. 2-8 High-power photograph shows immature blue bone in septa. Stromal cells show round to oval nuclei without atypism (hematoxylin–eosin stain, ×200).

RADIOLOGY

Radiography and CT

• Expansile cystic mass with a honeycomb or a soap bubble appearance around the pedicle (Fig. 2-9).
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