Solitary osteochondroma is a cartilage-capped bony projection on the external surface of a bone near the growth plate. It is considered a non-neoplastic anomaly similar to hamartoma. A neoplastic swelling means there is abnormal cell growth. However, it is a kind rather an overgrowth of the cartilage and bone.
These are located adjacent to growth plates and grow away from growth plate as natural bone growth occurs.
They stop growing after skeletal maturity.
It can occur as a solitary lesion or as multiple hereditary exostoses.
Solitary osteochondroma is a developmental anomaly of bone that results in the formation of an outgrowth on the surface of the bone. Other terms applied include osteocartilaginous exostosis and simple exostosis.
Multiple hereditary exostoses is an autosomal dominant hereditary disorder characterized by the presence of multiple osteochondromas associated with deformities of the bones affected.
Osteochondromas are usually classified as benign bone tumors, but they are not neoplastic in nature. They appear to result from aberrant epiphyseal development with a displacement of physeal cartilage and subsequent growth at right angles to the long axis of the bone.
In the simplest definition, osteochondroma is a cartilage-capped bony projection on the external surface of a bone.
The most common occurrences are around the knee and proximal humerus. Other bones where it is most commonly are seen in the bones ilium and scapula.
Rarely, these are present in the spine, typically in the posterior elements of the cervical spine.
Osteochondroma is are in small tubular bones of the hands and feet, in the ribs, and in the vertebral column
Osteochondroma makes up about 20-50% of benign bone tumors and about 10% of bone tumors making it the most common tumor.
Malignant changes occur in less than 1% of solitary osteochondromas.
Solitary osteochondroma affects males, almost twice as common, as females. Most of them are reported in the adolescent age group [less than 20 years]
Osteochondroma grows until skeletal maturity. The growth generally stops once the growth plates fuse.
Types of Solitary Osteochondroma
Solitary Osteochondroma is of two types
- Pedunculated- the one that has a stalk
- Sessile- the one with a broad base of attachment
Causes and Pathophysiology
The majority of solitary osteochondromas are sporadic lesions that occur. Secondary osteochondromas also occur and can develop after external radiation.
These are also known to occur after Salter-Harris fractures and physeal surgeries.
The exact cause is not known. It is thought to result from herniation of the peripheral portion of the physis resulting in an abnormal extension.
These have been found to have EXT1 and EXT gene mutations. Abnormal micro RNA expression has also been reported.
The osteochondroma grows away from the growth plate. They respond to, various growth factors and hormones in the same manner as epiphyseal growth plates do.
When we look at it grossly, the lesion looks like a lobulated cartilage cap 2mm to 1cm thick, covered by a fibrous membrane that is continuous with the periosteum covering the stalk.
It grows during childhood and adolescence by endochondral calcification.
The bursa may form at the periphery and be lined by synovium.
It may show inflammatory changes and in some cases, chondroid metaplasia.
Chondroid metaplasia may cause numerous cartilaginous loose bodies. When calcified these may simulate secondary chondrosarcoma on radiographs.
Locations
The lower limb is responsible for about half of the cases.
Different bones account for the numbers as follows
- Femur- 30% [distal femur most common]
- Tibia- 20% [proximal tibia most common]
- Humerus: 10-20% [Proximal humerus most common]
- Cervical spine
Clinical Presentation
Small growths may remain unnoticed for a long period.
Solitary ones grow as skeletal growth occurs.
The typical presentation is painless hard swelling in the metaphyseal area that might have increased in size over a few years.
Other presenting symptoms are
- a fracture of the osteochondroma
- Pressure on an adjoining structure like a vessel or nerve.
- A bursa may be present over the cap.
Sometimes, the bursa may become inflamed or accumulate synovial fluid or loose bodies and leading to painful swelling.
Pain might occur due to pressure on adjacent tissues like tendon, muscle, nerve, bursal inflammation, or a fracture of the osteochondroma.
A palpable mass is usually the only finding on clinical examination. Long-standing lesions may lead to angular deformities of the bone or limb-length discrepancies.
Lesions that occur near the joint may cause restriction of motion. In the spine, the symptoms secondary to cord or root compression may occur.
Differential Diagnosis
- Parosteal osteosarcoma [in c/o sessile type]
- Juxtacortical myositis
- Periosteal chondroma
Imaging
X-ray
On radiographs, osteochondromas can be sessile or pedunculated (have a stalk). The lesion typically arises from the metaphysis of a long bone, with a stalk that is continuous with the adjacent cortex and is oriented away from the epiphysis [the nearest joint].
Sessile lesions demonstrate a flat, plateau-like protuberance.
The rest of the bone is typically normal. Often slight localized distortion of the contour at stalk’s base end is visible [compare with changes of growth disturbance ] in multiple hereditary exostoses.
Usually, clinical examination and x-ray are sufficient to diagnose these lesions.
CT/MRI
In cases of doubt, CT and MRI are excellent imaging modalities.
MRI can help to measure the thickness of the cartilaginous cap but it is often not required.
MRI may be needed in large sessile osteochondromas difficult to distinguish from other cartilage-containing bone surface lesions.
Treatment
Osteochondromas are benign lesions with self-limited growth that ceases after skeletal maturity.
Most of them are left as such as they do not cause any symptoms. This lesion is almost always needs to be operated on for its complications [and not because lesion is there] which include
- Painful lesion
- Pressure effects
- Restriction of motion
- Compression on adjacent structures
- Deformity of the bone
- Fracture
- Bursitis
- Malignancy.
In such cases, complete removal of the lesion is sought.
An incomplete removal may lead to recurrence.
Recurrence after surgical excision is rare but may develop when a portion of cartilage cap or attached, perichondrium is left.
Malignant Changes
Malignant change in osteochondroma almost never occurs in growing age. As such malignant change is not very common but it does occur in adulthood to an incidence of 1%.
The most common associated malignancy is chondrosarcoma, although malignant fibrous histiocytoma and osteosarcoma have been reported.
High-grade sarcomas develop rarely in multiple hereditary exostoses
Lesions in the pelvis, scapula, ribs, and spine (Central Lesions) carry a higher risk of malignant transformation.
The reported risk for solitary osteochondromas is 1- 2% and 5-25% for multiple.
Signs suggestive of malignancy are
- A sudden increase in size
- Sudden onset of pain at the site
- Radiographic signs
- Areas of lucency
- Calcification in overlying soft tissue mass
- Destruction of the base or adjacent bone [Definite sign]
Radiographic changes may be difficult to ascertain in large sessile osteochondromas.
Most secondary tumors show the features of grade 1 to 2 chondrosarcoma. High-grade sarcomas may develop in the stalk or base of the lesion and invade adjacent bone and soft tissue.
Treatment is wide excision of the entire lesion with a surrounding rim of normal tissue.
References
- Mavrogenis AF, Papagelopoulos PJ, Soucacos PN. Skeletal osteochondromas revisited. Orthopedics. 2008 Oct. 31 (10). [Link]
- Heinritz W, Hüffmeier U, Strenge S, Miterski B, Zweier C, Leinung S, et al. New mutations of EXT1 and EXT2 genes in German patients with Multiple Osteochondromas. Ann Hum Genet. 2009 May. 73 (Pt 3):283-91.
- Tepelenis K, Papathanakos G, Kitsouli A, Troupis T, Barbouti A, Vlachos K, et al. Osteochondromas: An Updated Review of Epidemiology, Pathogenesis, Clinical Presentation, Radiological Features and Treatment Options. In Vivo. 2021 Mar-Apr. 35 (2):681-691.
