Chondroma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2], Farima Kahe M.D. [3], Soujanya Thummathati, MBBS [4]

Juxtacortical chondroma was first discovered by Lichtenstein and Hall in 1952. The term juxtacortical chondroma was first coined by Jaffe in 1956. Chondroma may be classified according to location of the outgrowth into 3 groups that include enchondrom, periosteal chondroma and synovial chondroma. Enchondromas arise from rests of growth plate cartilage or chondrocytes that are normally involved in the production and maintainence of the cartilaginous matrix, which consists mainly of collagen and proteoglycans. Genes involved in the pathogenesis of enchondromas and periostal chondromas include isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2). On gross pathology, small (usually less than 3 cm), translucent, grey blue, nodular lesions with occasional calcifications are characteristic findings of chondromas. Enchondromas may be single or multiple. Multiple enchondromas are associated Maffucci syndrome, Ollier disease and metachondromatosis. The cause of chondromas has not been identified. However, enchondroma is believed to occur either as an overgrowth of the cartilage that lines the ends of the bones, or as a persistent growth of original embryonic cartilage.The incidence of osteochondromas is approximately 30,000 per 100,000 of all cartilage tumors and 2,000 per 100,000 of all bone tumors.The prevalence of enchondromas is approximately 12,000 – 24,000 per 100,000 individuals of benign bone tumors and 3000 – 10,000 of all bone tumors. Patients of all age groups may develop enchondromas. The incidence of enchondroma peaks in the third and fourth decades of life. Enchondroma affects men and women equally. Chondroma is usually diagnosed incidentally. Common complications of chondroma include malignant transformation into a low grade growth disturbance, pathologic fracture, especially in short tubular and recurrence. Benign chondromas have a good prognosis with aprropriate treatment. The majority of patients with enchondroma are asymptomatic. Less common symptoms of enchondroma may include pain, enlargement of the affected digits, and slowing of affected bone growth and asymmetrical bone deformities. There are no diagnostic lab findings associated with chondroma. Findings on an x-ray suggestive of chondroma include well-defined or sclerotic border, sharp zone of transition, confinement by natural barriers, lack of destruction of the cortex and lack of extension into the soft tissue. Findings on CT scan suggestive of enchondroma include sharply defined scalloped margins, expansion of the overlying cortex may be present, no periosteal reaction and soft tissue mass. Findings on MRI suggestive of chondroma include well circumscribed, lobulated mass replacing the marrow for enchondroma, lobulated soft tissue lesion that is abutting the cortex and evidence of pressure erosion on neighboring bone, with no evidence of medullary bone or soft tissue edema for periostal chondroma for periostal chondroma. Surgery is not the first-line treatment option for patients with asymptomatic and benign chondroma. Surgery is usually reserved for patients with either malignant transformation and pathological fracture.

Juxtacortical chondroma was first discovered by Lichtenstein and Hall in 1952. The term juxtacortical chondroma was first coined by Jaffe in 1956.

Chondroma may be classified according to location of the outgrowth into 3 groups that include enchondrom, periosteal chondroma and synovial chondroma.

Enchondromas arise from rests of growth plate cartilage or chondrocytes that are normally involved in the production and maintainence of the cartilaginous matrix, which consists mainly of collagen and proteoglycans. Genes involved in the pathogenesis of enchondromas and periostal chondromas include isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2). On gross pathology, small (usually less than 3 cm), translucent, grey blue, nodular lesions with occasional calcifications are characteristic findings of chondromas. Enchondromas may be single or multiple. Multiple enchondromas are associated Maffucci syndrome, Ollier disease and metachondromatosis.

The cause of chondromas has not been identified. However, enchondroma is believed to occur either as an overgrowth of the cartilage that lines the ends of the bones, or as a persistent growth of original embryonic cartilage.

The incidence of osteochondromas is approximately 30,000 per 100,000 of all cartilage tumors and 2,000 per 100,000 of all bone tumors.The prevalence of enchondromas is approximately 12,000 – 24,000 per 100,000 individuals of benign bone tumors and 3000 -10,000 of all bone tumors. Patients of all age groups may develop enchondromas. The incidence of enchondroma peaks in the third and fourth decades of life. Enchondroma affects men and women equally.

There are no established risk factors for chondromas.

There is insufficient evidence to recommend routine screening for chondromas.

Enchondroma must be differentiated from low-grade chondrosarcoma, fibrocartilaginous dysplasia, bone islands and bone infarcts. Periosteal chondroma must be differentiated from periosteal chondrosarcoma and periosteal osteosarcoma.

Chondroma is usually diagnosed incidentally. Common complications of chondroma include malignant transformation into a low grade growth disturbance, pathologic fracture, especially in short tubular and recurrence. Benign chondromas have a good prognosis with aprropriate treatment.

The majority of patients with enchondroma are asymptomatic. Less common symptoms of enchondroma may include pain, enlargement of the affected digits, and slowing of affected bone growth and asymmetrical bone deformities.

Patients with chondroma usually appear well. Physical examination of patients with enchondroma is usually unremarkable.

There are no diagnostic lab findings associated with chondroma.

There are no electrocardiogram findings associated with chondroma.

Findings on an x-ray suggestive of chondroma include well-defined or sclerotic border, sharp zone of transition, confinement by natural barriers, lack of destruction of the cortex and lack of extension into the soft tissue.

Findings on CT scan suggestive of enchondroma include sharply defined scalloped margins, expansion of the overlying cortex may be present, no periosteal reaction and soft tissue mass.

Findings on MRI suggestive of chondroma include well circumscribed, lobulated mass replacing the marrow for enchondroma, lobulated soft tissue lesion that is abutting the cortex and evidence of pressure erosion on neighboring bone, with no evidence of medullary bone or soft tissue edema for periostal chondroma for periostal chondroma.

There are no echocardiography or ultrasound findings associated with chondroma.

Other imaging studies for enchondroma includes radionuclide bone scan.

There is no medical therapy for chondromas; the mainstay of therapy is surgery.

Surgery is not the first-line treatment option for patients with asymptomatic and benign chondroma. Surgery is usually reserved for patients with either malignant transformation and pathological fracture.

There is no established method for primary prevention of chondroma.

There is no established method for secondary prevention of chondroma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Farima Kahe M.D. [2], Soujanya Thummathati, MBBS [3]

Juxtacortical chondroma was first discovered by Lichtenstein and Hall in 1952. The term juxtacortical chondroma was first coined by Jaffe in 1956.

• Juxtacortical chondroma was first discovered by Lichtenstein and Hall in 1952. It was initially termed periosteal chondroma.
• The term juxtacortical chondroma was first coined by Jaffe in 1956.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2], Farima Kahe M.D. [3], Soujanya Thummathati, MBBS [4]

Chondroma may be classified according to location of the outgrowth into 3 groups that include enchondroma, periosteal chondroma and synovial chondroma.

• Chondroma may be classified according to location of the outgrowth into 3 groups:^[1][2][3]
  • Enchondroma
  • Periosteal chondroma
  • Synovial chondroma

• Another classification for chondroma which is used less commonly is based on their anatomic locations:^[4][5][6]
  • Chondroma of tip of the nose
  • Extraskeletal chondroma of the scalp
  • Intracranial chondroma
  • Sacrococcygeal chondroma
  • Skull base chondroma
  • Spinal chondroma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2] Farima Kahe M.D. [3], Soujanya Thummathati, MBBS [4]

Enchondromas arise from rests of growth plate cartilage or chondrocytes that are normally involved in the production and maintenance of the cartilaginous matrix, which consists mainly of collagen and proteoglycans. Genes involved in the pathogenesis of enchondromas and periosteal chondromas include isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2) . On gross pathology, small (usually less than 3 cm), translucent, grey blue, nodular lesions with occasional calcifications are characteristic findings of chondromas. Enchondromas may be single or multiple. Multiple enchondromas are associated Maffucci syndrome, Ollier disease and metachondromatosis.

• Enchondromas arise from rests of growth plate cartilage or chondrocytes that are normally involved in the production and maintenance of the cartilaginous matrix, which consists mainly of collagen and proteoglycans.^[1]
• Chondromas arise as the result of nests of growth plate cartilage that have become entrapped in the medullary canal of the metaphysis or in the metaphyseal–diaphyseal junction. These hamartomatous proliferations persist as islands in the bone and then develop from enchondral ossification.^[2][3]

• Genes involved in the pathogenesis of enchondromas and periosteal chondromas include isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2) .^[4]

Enchondromas may be single or multiple. Multiple enchondromas are associated with the following:^[5][6][7]

• On gross pathology, small (usually less than 3 cm), translucent, grey blue, nodular lesions with occasional calcifications are characteristic findings of chondromas.^[8][9]

• On microscopic histopathological analysis, characteristic findings of chondroma are as followings:^[10][11]
  • Cytologically benign cells in spaced nests
  • Not extending into surrounding soft tissue
  • Avascular, fibrous lobules of hyaline cartilagenous matrix
  • Interspersed with chondrocytes and separated by normal marrow

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2], Soujanya Thummathati, MBBS [3]

The cause of chondromas has not been identified.

• The cause of chondromas has not been identified. Fibroblast growth factor receptor (FGFR3) deletion may be induced multiple chondroma-like lesions, including enchondromas and osteochondromas.^[1]
• However, enchondroma is believed to occur either as:
  • An overgrowth of the cartilage that lines the ends of the bones
  • A persistent growth of original embryonic cartilage.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2], Farima Kahe M.D. [3], Soujanya Thummathati, MBBS [4]

The incidence of otesochondromas is approximately 30,000 per 100,000 of all cartilage tumors and 2,000 per 100,000 of all bone tumors.The prevalence of enchondromas is approximately 12,000 – 24,000 per 100,000 individuals of benign bone tumors and 3000-10,000 of all bone tumors. Patients of all age groups may develop enchondromas. The incidence of enchondroma peaks in the third and fourth decades of life. Enchondroma affects men and women equally.

• The incidence of otesochondromas is approximately 30,000 per 100,000 of all cartilage tumors and 2,000 per 100,000 of all bone tumors.^[1]

• The prevalence of benign cartilage tumors is approximately 27000 per 100,000 individuals of all bone tumors and 70,000 per 100,000 of all cartilage tumors.^[2][3]
• The prevalence of enchondromas is approximately 12,000 – 24,000 per 100,000 individuals of benign bone tumors and 3000-10,000 of all bone tumors.^[4]
• The prevalence of periosteal chondromas is approximately 1000 per 100,000 individuals of all chondromas and 100 per 100,000 of all bone tumors.

• Patients of all age groups may develop enchondromas.
• The incidence of enchondroma peaks in the third and fourth decades of life.^[5]
• Periosteal chondromas are frequently diagnosed in the second or third decades of life.
• Patients of all age groups may develop synovial chondromas, and fifth decade is a peak incidence.^[6]

• There is no racial predilection to chondroma.

• Enchondroma affects men and women equally.
• Males are more commonly affected by periosteal chondromas than females.^[7]
• Male are more commonly affected by osteochondromas than female. The male to female ratio is approximately 1.8 to 1.^[7]
• Male are more commonly affected by synovial chondroma than female.The male to female ratio is approximately 2 to 1.^[8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2], Soujanya Thummathati, MBBS [3]

There are no established risk factors for chondroma.

There are no established risk factors for chondroma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soujanya Thummathati, MBBS [2]

There is insufficient evidence to recommend routine screening for chondromas.

There is insufficient evidence to recommend routine screening for chondromas.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Rohan A. Bhimani, M.B.B.S., D.N.B., M.Ch.[2]

Enchondroma must be differentiated from low-grade chondrosarcoma, fibrocartilaginous dysplasia, bone islands and bone infarcts. Periosteal chondroma must be differentiated from juxtacortical chondrosarcoma, osteochondroma and periosteal osteosarcoma.

Enchondroma must be differentiated from the following:^[1][2]

• When differentiating an enchondroma from a chondrosarcoma, the radiographic image may be equivocal. However, periostitis is not usually seen with an uncomplicated enchondroma.

• Presence of bone marrow edema frequently seen surrounding chondroblastomas is helpful, as it is not a usual feature of chondromyxoid fibromas, giant cell tumors, or enchondromas.^[1]

• Fibrous dysplasia is seen with an extensive cartilagenous differentiation that results in a picture that mimics enchondroma.
• Cellular atypia in the surrounding stroma helps in the differentiation.^[2]

• Small focus of compact bone within the cancellous bone.
• No cortical destruction or involvement of the surrounding soft tissues.

• Differentiating an enchondroma from a bone infarct on plain film may be difficult.
• An enchondroma usually causes endosteal scalloping while an infarct will not.
• An infarct usually has a well-defined, sclerotic serpentine border, whereas an endochondroma does not have a well defined border.

Periosteal chondroma must be differentiated from the following:^[3][4][5][6]

• Chondrosarcomas are generally greater in size and occur in older patients more than 50 years of age.
• They may extend into the soft tissue.
• Periosteal chondrosarcoma shows popcorn calcifications on radiographs, which present as a collection of scalloped radiolucencies and with a sclerotic margin.

• Periosteal osteosarcomas are slow-growing, and primarily arise beneath the periosteum, inducing new bone formation.
• It seen as a radiolucent lesion on the bone surface with perpendicular striae and a peripheral Codman’s triangle on radiography.

• Osteochondromas are more commonly seen in adolescents, in contrast with periosteal chondromas, which typically occur in young adults.
• Osteochondromas may also be distinguished by the presence of a dense osteoid formation in the cortex and medulla of the mass, and by the continuation with its originating bone.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2], Soujanya Thummathati, MBBS [3]

Chondroma is usually diagnosed incidentally. Common complications of chondroma include malignant transformation into a low grade growth disturbance, pathologic fracture, especially in short tubular bones and recurrence. Benign chondromas have a good prognosis with appropriate treatment.

• Chondroma is usually diagnosed incidentally.^[1]
• Chondroma grows slowly, with a mean time of 41 months between initial diagnosis and change in lesion.

• Common complications of chondroma include:^[2][3][4][5]
  • Malignant transformation into a low grade chondrosarcoma
  • Growth disturbance
  • Pathologic fracture, especially in short tubular bones
  • Recurrence

• Benign chondromas have a good prognosis with aprropriate treatment.^[6]
• Most patients with chondroma under treatment remain asymptomatic and the disease may rarely recur.^[7]

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