Monday, 8 February 2016

Osteoblastoma of Spine


In 1935 Jaffe described a new bone lesion , which he named osteoid osteoma.  In 1956, Jaffe and Lichenstein independently proposed the term “ benign osteoblastoma”. Osteoid osteoma and osteoblastoma are bone producing lesions that are frequently localized in long bones and posterior elements of the vertebra1-5.

Primary osseous tumors of the spine are uncommon  lesions that are much less frequently encountered than metastases, multiple myeloma, and lymphoma4. Osteoid osteoma (OO) and osteoblastoma ( OB) are rare primary bone tumors that usually do not arise in the spine4.

Benign osteoblastoma is a very rare lesion presenting 1 percent of all primary bone tumors. Osteoblastoma is histologically similar to osteoid osteoma, but Osteoblastoma  occurs in slightly older patients, has a greater propensity for the spine and more aggressive , often eroding through spinal cortical bone and creating large soft tissue masses. Some distinguish the two based on size with lesions less than 1.5 cm classified as Osteoid Osteoma , and those larger than 1.5 cm are considered Osteoblastoma6,7. Moreover, Osteoblastoma  of the spine may have soft tissue masses, which initially may encroach on the spinal canal and later may surround the dural sac or adjacent nerve roots or both4. Osteoblastomas  occur predominantly in patients younger than 20 years of age. Clinically, the pain of Osteoblastoma is not as severe at night, nor is it relieved by aspirin or NSAIDs , as is the pain of Osteoid Osteoma. Unlike osteoid osteoma no spontaneous regression has been reported with osteoblastoma8.

When these lesions occur in the spine,  common manifestations are pain, scoliosis and neurological involvement4,9.  The primary histologic difference between Osteoid Osteoma & Osteoblastoma is the tendency of OB to form a less sclerotic but more expansile mass. The nidus characteristic of OO is not found in OB. Also, large vascular spaces seen in OB are rare in OO4.

On histological examination osteoid osteoma consists of small yellowish to red nidus of the osteoid and woven bonewith interconnected trabeculae, and a background and rim of highly vascularised fibrous connective tissue. Varying degrees of sclerotic bone reaction may surround the lesion4.

Benign osteoblastoma is virtually indistinguishable from osteoid osteoma. The usual appearance included a fibrovascular stroma with numerous osteoblasts, osteoid tissue, well formed woven bone, and giant cells.4. Osteoblastomas have an abundantly vascularised stroma containing a great number of very active osteoblasts ( creating osteoid and primitive osseous trabeculae with somewhat more regular orientation). Osteoblasts are usually larger with atypical nuclei and more frequent and somewhat pathological mitoses. Mineralization of bone trabeculae is uneven and irregular, osteoblasts are numerous especially around the zones of hemorrhage5.

In a histological aggressive osteoblastoma bone trabeculae are broad and irregular. The deposited osteoid is usually stacked in layers ( lamelated) but not trabeculated. Swollen, enlarged osteoblasts coating trabeculae or osteoid are a typical feature. The stroma is fibrous, made of spindle cells, with an increased cellularity and focus whirling cellular agglomerations5.

Patients of osteoblastoma usually present with back pain. Patients may also present with progressive focal or radicular pain exacerbated by movement. The other common symptom is stiffness. The  time from onset of symptoms to diagnosis is typically several months because it is rare entity and radiographic studies are often negative early in the course of the disease6. Many patients will progress to manifest neurological sequelae or a painful scoliosis6.

 The plain x-ray, CT scan and MRI aid in the diagnosis. Radigraphically the tumor is often radiolucent. On x-rays osteoid osteomas are usually about 2 cm size with a sclerotic rim and osteoblastomas are usually  larger in size. Both osteoid osteoma and osteoblastomas are more common in posterior elements occurring predominantly in the pedicles, transverse processes, lamina and spinous processes. Osteoblastomas may have soft tissue masses, which initially may  encroach on the spinal canal and later may surround the dural sac or adjacent nerve roots, or both4. Extent of the osseous involvement is assessed by x-ray and CT scan of the spine. MRI reveals the nidus,  intra- and extraosseous reactive changes and the possible infiltration of adjeacent soft tissues. MRI is the best to show the effects of the tumor on the spinal canal and cord4.

Technitium bone scanning may accurately localize the lesion as it demonstrates an intense focal accumulation of the bone seeking agent. The site of the tumor appears as a typical “ hot spot” on a technetium bone scan.But, if lesion is already discernible on x-ray films, the scintigram is unnecessary4.

Surgery is the most common treatment for this disease, and prognosis after total resction is favourable.The recommended treatment is excision. Most OB are multilobular with extension into the  paraspinal mass may not allow en bloc resections. Recurrence is the result of incomplete resection . these lesions hardly ever undergo malignat transformation into osteosarcoma and metastasize. Differentiation between these tumor and fibrous dysplasia , osteosarcoma, giant cell bone tumor, or aneurismal bone cyst is necessary which usually have different radiology and histology4.

Lesions may be  well-circumscribed margins confined within the vertebral structure (Enneking Stage 2), or ill-defined margins with soft-tissue extension (Enneking Stage 3). The staging system for benign musculoskeletal tumors based on radiographic characteristics consists of three categories: ie, latent, active, and aggressive. Latent means lesions with well demarcated borders, active lesions have indistinct borders and aggressive lesions reveal indistinct borders on radiography. Well-defined lesions are treated with curettage, with excellent results. The more extensive lesions are treated by intralesional excision and adjuvant radiation therapy10,11.  

So, the well-defined lesions are excised or removed completely with curettage. The more extensive lesions were treated by intralesional excision and adjuvant radiation therapy9.

There are few data about the effectiveness of chemotherapy or radiotherapy in the treatment of recurrent osteoblastoma. Surgery remains the treatment of choice for osteoblastoma. Radiotherapy and chemotherapy either alone or together may be useful in selected patients with recurrent, aggressive tumor or in patients with surgically unresectable disease12.

Resection of the tumor may be done either through the anterior approach or posterior approach depending upon the location of the tumor in the vertebra. Surgical approaches, bone grafting , implants and spinal fixation may also vary depending upon the site of the lesion in vertebral column.

So, to achieve the safe resection many studies have been published in English literature, highlighting the modern technologies and multimodality approaches. Samsadi et al proposed the preoperative angiography to confirm hypervascularity of the lesion and consequent embolization and resection6.

The resection of the abnormal pedicle, transverse process, pedicle and facet joint may lead to instability of the spine and requires spinal stabilization with instrumentation.Video assisted thoracoscopic surgery (VATS)  and  Video assisted thoracoscopic surgery guided by a navigation system ( VATS-NAV) allows accurate localization and guidance for complete excision of a spinal osteoid osteoma through a minimally invasive approach without compromising spinal stability13.

An underlying osteoid osteoma and osteoblastoma must be suspected in all young patients presenting with pain, painful scoliosis and stiffness. Early diagnosis is possible with x-ray, CT scan, MRI and technetium bone scan. Early diagnosis and treatments prevents scoliosis & permits complete resection without jeopardizing the stability of the spine14.

 

References

  1. Jaffe HL, Mayer L. An osteoblastic osteoid tissue-forming tumor of a metacarpal bone. Arch Surg. 1932;24:550–564.
  2. Jaffe HL. Benign osteoblastoma. Bull Hosp Joint Dis. 1956;17:141–151
  3. Lichtenstein L. Benign osteoblastoma : a category of osteoid- and bone-forming tumors other than classical osteoid osteoma, which may be mistaken for giant-cell tumor or osteogenic sarcoma. Cancer. 1956;9:1044–1052.
  4. Zileli M, ÇAGL S, BASDEMIR G, ERSAHIN Y . Neurosurg Focus 15 (5):Article 5, 2003,1-6.
  5. Poleksi Z. R., Lalosevic V. J., Milinkovi Z. B. Osteoblastoma of spine ACI Vol. LVII , 63-68.  

  1. Samsadani A, Torre-Healy A, Chou D, Cahill AM, Storm P B. Treatment of osteoblastoma at C7: a multidisciplinary approach. A case report and review of literature. Eur Spine J ( 2009) 18 ( Suppl 2): S196-S200.
  2. Mc Cleod RA , Dahlin DC, Beabout JW (1976) The spectrum of osteoblastoma . AJR Am J Roentgenol 126;321-325
  3. Peivandi M T, Ameri E, Ganjavian S, Behtash H, Mobini B. Osteoblastoma of the spine. MJIRC, Vol.8, No.1, May 2005,52-56.
  4. Boriani S, Capanna R, Donati D, Levine A, Picci P, Savini R. Osteoblastoma of the spine. Clin Orthop Relat Res. 1992 May;(278):37-45.
  5. Javad M U, Scully S P. Enneking classification: Benign and manalignat tumors of the musculoskeletalsystem. Clin Orthop Relat Res (2010), 468: 2000-2002
  6. Enneking WF, Spanier SS, Goodman MA. A system for the surgical staging of musculoskeletal sarcoma.1980. Clin Orthop Relat Res. 2003;415; 4-18
  7. Berberoglu S, Oguz A, Aribal E, Ataoglu O. Osteoblastoma response to radiotherapy and chemotherapy. Med Pediatr Oncol. 1997 Apr;28(4):305-9.
  8. Alessandro Gasbarrini , Stefano boriani, Case report: curetting OO of the spine using combined video-assisted thoracoscopic surgery and navigation . Clinical Orthopedics and related research, Feb 2013, vol 471, issue2, 680-685.
  9. Kirwan E.O’G, Hutton P A N, Pozo J L, Ransford A O, Osteoid osteoma and benign osteoblastoma of the spine. Clinical presentation and treatment. The Journal of Bone and Joint Surgery, Vol.66-B, No.1, January 1984, 21-26.

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