Osteoid osteoma

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For more information about osteoma that is not associated with osteoid osteoma, see osteoma Template:Osteoid osteoma Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maria Fernanda Villarreal, M.D. [2]

Synonyms and keywords: Osteoma osteoid; OO; Osteoid osteomas

Historical Perspective

• In 1930, Dr. Bergstrand, a German physician, first described osteoid osteoma in 1930.
• In 1935, Dr.Henry Jaffe, an American pathologist first described osteoid osteoma as a benign bone tumor.
• In 1953, Dr. Jaffe coined the term nidus, which was described as the “core”, referring to the tumor itself and is composed of bone at various stages of maturity within a highly vascular connective tissue stroma.
• In 1954, Dahlin and Johnson added the term giant osteoid osteomas.
• In 1966, Dr.Edeiken classifed osteoid osteomas into three types.

Classification

• Osteoid Osteoma can be classified based on location and imaging findings.

Anatomical Classification

• Based on Location:

Type of osteoid osteoma	Characteristics
Intracortical	Dense sclerosis around the nidus
Periosteal	Periosteal reaction
Cancellous (medullary)	Produces very little reactive bone
Subarticular	Simulates arthritis as it produces synovial reactions

Enneking (MSTS) Staging System

• The Enneking surgical staging system (also known as the MSTS system) for benign musculoskeletal tumors based on radiographic characteristics of the tumor host margin.
• It is widely accepted and routinely used classification.

Stages	Description
1	Latent: Well demarcated borders
2	Active: Indistinct borders
3	Aggressive: Indistinct borders

Pathophysiology

• The exact etiology of osteoid osteoma is unknown.
• Osteoid osteoma arises from the osteoblasts.
• Osteoid osteoma consists of radially oriented trabeculae of surrounding reactive bone, indicating an increased pressure in the vascular nidus.
• This arrangement of the bony trabeculae is due to the stresses placed on them.
• This increased pressure is due to vasodilatation and edema is which stimulate intraosseous nerve endings, generating pain.
• In addiition, the pain is also attributed to increased local concentration of prostaglandin E2, COX1 & 2 expression; and increased number and size of unmyelinated nerve fibers within the nidus.
• Osteoid osteomas are usually cortical lesions but they can occur anywhere within the bone including medullary, subperiosteal (most common in talus), and intracapsular area.
• More than 50 percent of osteoid osteomas occur in lower extremity of long bones.
• It most commonly affects the metadiaphysis of the femur and tibia.
• About 20 percent of osteoid osteomas occur in the posterior elements of the spine.

Genetics

• The structural chromosomal alterations involving 22q13.1 in osteoid osteoma may affect critical genes involved in the regulation of cell proliferation, such as the YWHAH gene.
• YWHAH gene codes for a 14-3-3 family members of dimeric phosphoserine-binding proteins that participate in signal transduction and checkpoint control pathways.
• Their primary function is to inhibit apoptosis.
• Another gene mapped in this region is PDGFB that codes for a platelet-derived growth factor, a beta polypeptide (simian sarcoma viral [v-sis] oncogene homolog), a potent mitogen for cells of mesenchymal origin and involved in the transformation process.

Causes

• The cause of osteoid osteoma has not been identified.

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Epidemiology and Demographics

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Diagnosis

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Physical Examination

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Laboratory Findings

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Electrocardiogram

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X-ray

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Echocardiography or Ultrasound

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CT scan

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MRI

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Treatment

Medical Therapy

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Surgery

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Primary Prevention

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Secondary Prevention

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References

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