= OSTEOCARTILAGINOUS EXOSTOSIS

= developmental hyperplastic / dysplastic bone outgrowth composed of cortical + medullary bone with overlying cartilaginous cap; growth ends when nearest epiphyseal plate fuses

◊Most common benign growth of the skeleton!

◊Most common benign cartilage-containing tumor!

Prevalence: 20–50% of all benign bone tumors; 10% of all bone tumors

Etiology: separation of a fragment of physeal cartilage herniating through periosteal bone cuff that surrounds the growth plate (encoche of Ranvier); the fragment continues to grow and undergoes enchondral ossification

1. developmental
2. microtrauma / Salter-Harris injury with in vivo transplantation of physeal tissue
3. radiation therapy (in 6–24%) with latency period of 3–17 years in patients between 8 months and 11 years of age receiving 1,500–5,500 cGy (frequently for treatment of neuroblastoma / Wilms tumor); at periphery of radiation field
   • Most common benign radiation-induced tumor

Path: continuity of lesion with marrow + cortex of host bone (HALLMARK)

Histo: hyaline cartilage cap containing a basal surface with enchondral ossification (thin cortex + trabecular bone + marrow space) resembling growth plate

Location: 10% in small bones of the hands and feet; 1–4% in spine (50% in posterior elements of cervical spine)

• progressive painless deformity around a joint
  Radiographic types:
  • sessile broad based exostosis
  • pedunculated with slender stalk / pedicle:
    • growth pointing away from nearest joint + toward center of shaft:
      • at right angle on diaphyseal side of stalk
      • slope on epiphyseal side
• continuity of bone cortex with host bone cortex
• continuity (!) of medullary marrow space with host bone
• hyaline cartilaginous cap:
  • arcs / rings / flocculent calcifications on radiographs

CT:

• optimal depiction of cortical + marrow continuity with host bone (PATHOGNOMONIC) by CT
• nonmineralized cartilage cap hypodense to muscle (in 75–80%):
  • 6–8 mm thick in skeletally mature patients
  • up to 30 mm thick in skeletally immature patients

MR (best modality):

• cortical + medullary continuity:
  • peripheral rim of low signal intensity = cortical bone
• hyaline cartilage cap very hyperintense on T2WI + of low to intermediate intensity on T1WI ← high water content:
  • central area of fat signal intensity = cancellous bone
  • smooth continuous appearance with relatively thin cap
  • hypointense mineralized areas of cartilage
  • hypointense periphery = perichondrium
  • slight septal + peripheral enhancement
• cartilage tends to thin and disappear at numerous points on surface of osteochondroma

US:

• hypoechoic nonmineralized cartilaginous cap easily distinguished from muscle and fat
• posterior acoustic shadowing for mineralized portion

NUC:

• active lesion (predominantly in young patient)
• quiescent lesion in older patient

Prognosis: exostosis begins in childhood; stops growing when nearest epiphyseal center fuses after skeletal maturity

Rx: surgical excision (2% recurrence rate, 13% complication rate [neuropraxia, arterial laceration, compartment syndrome, fracture])

Cx:

1. Osseous and cosmetic deformity (most frequent)
   • mechanical limitation of joint movement
   • snapping tendon / ligament
   • hematuria (irritating pubic osteochondroma)
   • saucerization / scalloping of cortex of adjacent bone due to extrinsic pressure erosion (of paired tubular bones)
   • premature osteoarthritis
   • pleural effusion / spontaneous hemothorax ← irritating rib lesion
2. Fracture through stalk of osteochondroma
3. Vascular compromise
   • venous / arterial stenosis
   • arterial occlusion / venous thrombosis
   • pseudoaneurysm formation:
     • Cause: repetitive trauma to vessel wall
     • Age: near end of normal skeletal growth
     • Location: popliteal a., brachial a., superficial femoral a., posterior tibial a.
4. Neurologic compromise
   • peripheral nerve compression with entrapment neuropathy: foot drop with peroneal nerve involvement (most frequent)
   • central nerve compression: cranial nerve deficit, radiculopathy, cauda equina syndrome, cord compression with myelomalacia
     • often very narrow stalk of attachment
     • difficult imaging diagnosis owing to complex anatomy of skull base (21% TP)
     • spinal canal osteochondroma (15% FN)
5. Reactive bursa formation (in 1.5%)
   • enlarging mass overlying an osteochondroma simulating malignant transformation
   
   Location: scapula (>50%), lesser trochanter, shoulder
   • fluid-filled mass ± chondral filling defects:
     • mineralization of intrabursal chondral bodies may mimic a thick cartilage cap with growth
   
   Cx: inflammation, infection, hemorrhage into bursa, secondary synovial chondromatosis
6. Malignant transformation into secondary / peripheral chondrosarcoma / osteosarcoma
   Frequency: 1% in solitary osteochondroma; 3–5% in hereditary multiple osteochondromatosis
   Location: iliac bone commonest site
   Of concern: interval growth, indistinct cortical margins, erosion of lesion + adjacent parent bone, large soft-tissue component
   ◊Any cartilage cap >1.0–1.5 cm thick / continued growth after skeletal maturation is suspect of malignant transformation!