Periosteal reaction: Difference between revisions
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==Overview== | ==Overview== | ||
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*Bustein HJ, Janicek MJ, Skarin AT. Hypertrophic osteoarthropathy. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9215850 J Clin Oncol 1997;15(7):2759-2760]. | *Bustein HJ, Janicek MJ, Skarin AT. Hypertrophic osteoarthropathy. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9215850 J Clin Oncol 1997;15(7):2759-2760]. | ||
[[Category:Rheumatology]] | [[Category:Rheumatology]] |
Latest revision as of 14:55, 20 August 2012
Overview
Periosteal new bone formation or periosteal reaction can result from any of a large number of causes. The morphological appearance of periostitis (figure below) can be helpful, but is usually not sufficiently specific to determine its etiology. Establishing whether periosteal new bone formation is solitary versus multi-focal (or generalized) is useful in narrowing the diagnostic possibilities. Common causes of solitary periosteal new bone formation would include healing fractures, chronic stress injuries, subperiosteal hematomas (e.g., cephalohematoma), osteomyelitis, and bone tumors. The appearance of the adjacent bone will gives clues as to which of these is the most likely etiology.
Fig. 1 Schematic of different morphologies of periosteal reaction (after Resnick). (Upper left) single layer of new bone may be seen in benign or malignant tumors, infection, and secondary hypertrophic osteoarthropathy. (Upper mid) multiple layers - "onion skinning" - of new bone may be seen in hypertrophic osteoarthropathy, osteomyelitis, and tumors. (Upper right) irregular excrescences may be seen in hypertrophic osteoarthropathy, venous stasis, and thyroid acropachy. (Lower left) linear spicules are often associated with Ewing's sarcoma. (Lower mid) linear spiculates in a radial configuration - "sunburst" - are associated with osteosarcomas. (Lower right) linear new bone in a triangular configuration - "Codman triangle" - is suggestive of malignancy.
Generalized periosteal new bone formation is less frequently encountered and has its own differential diagnosis.
- Primary Hypertrophic Osteoarthropathy (Pachydermoperiostosis)
- Secondary Hypertrophic Osteoarthropathy
- Pulmonary - neoplasm, abscess, cystic fibrosis, mesothelioma
- Cardiac - cyanotic congenital heart disease (e.g., Tetrology of Fallot)
- Abdominal - Ulcerative colitis, Crohn's disease, cirrhosis, polyposis
- Chronic Venous Stasis
- Thyroid Acropachy
- Multi-focal Osteomyelitis
- Infantile Cortical Hyperostosis (Caffrey's Disease)
- Child Abuse
Radiologic Findings
Primary hypertrophic osteoarthropathy
Hypertrophic osteoarthropathy is a clinical syndrome that consists of clubbing of the digits, painful swollen joints, enlargement of the extremities due to osseus proliferation, and thickening of the skin over the face and scalp. An individual may have all or any combination of the above features. Primary hypertrophic osteoarthropathy is the hereditary forms and accounts for only 3-5% of all hypertrophic osteoarthropathy. It has autosomal dominant inheritance with variable expression. Radiographs demonstrate irregular or fluffy periosteal reaction that most often involves the long tubular bones of the extremities - radius, ulna, tibia, and fibula. The metacarpals, phalanges, and pelvis can also be involved. Resorption of the phalangeal tufts has also been described. In the primary form, the periostitis is usually not painful.
Fig. 2 Primary hypertrophic osteoarthropathy. Note diffuse periosteal new bone formation of the distal radius and ulna. The metcarpals are also affected.
Secondary hypertrophic osteoarthropathy
Secondary hypertrophic osteoathropathy is the acquired and has a high association with intrathoracic diseases (which explains why it was called hypertrophic pulmonary osteoarthropathy). It may occur in up to 5% of patients with bronchogenic carcinoma and up to 50% of patients with mesothelioma. Cardiac and gastrointestinal diseases, although frequent, also are associated with development of the disease. The mechanism by which these diverse conditions induce disease is unknown. Interestingly, in the cases of abscesses and lung cancer, it has been noted the patient's symptoms resolve within a day following thoracotomy. Clinically patients with the secondary form of the disease tend to have pain that is often worse at night. From a radiographic standpoint the periosteal reaction can be single- or multilayered-linear or irregular, such as with the primary form. Overall the distribution is similar to the primary form with a predilection for tubular long bones of the extremities.
Fig. 3 Secondary hypertrophic osteoarthropathy in a patient with a fungal infection.
Fig. 4 Secondary hypertrophic osteoarthropathy in a patient with lung neoplasm.
Periostitis
The frequency of periostitis increases with the duration and severity of chronic venous stasis; it is reported in 10-60% of patients. The radiographic findings tend to be distributed in the lower extremities of these patients from femur to the metatarsals.
Fig. 5 Periosteal new bone formation in a patient with chronic venous stasis.
Other Findings
Thyroid acropachy is uncommon. It manifests as periosteal new bone formation in the hands and less commonly in other tubular bones.
Caffrey's disease is an uncommon form of hyperostosis and periosteal reaction that occurs in newborns. There is usually very dense periosteal new bone formation. It can occur at any site, but the mandible, clavical, and scapula, and ribs are most commonly involved.
References
- Periosteal reaction: a differential diagnosis by David Coy, M.D., University of Washington Department of Radiology
- Resnick, D (1994) Diagnosis of Bone and Joint Disorders, 3rd ed (W.B. Saunders: Philadelphia) 4421-4445.
- Ved N, Haller JT (2002) Periosteal reaction with normal-appearing bone: a child abuse mimicker. Emerg. Radiol. 9(5):278-282.
- Marmur R, Kagen L (2002) Cancer-associated neuromusculoskeletal syndromes. Recognizing the rheumatic-neoplastic connection. Postgrad. Med. 111(4):95-98;101-102.
- Viola IC, Joffe S, Brent LH (2000) Primary hypertrophic osteoarthropathy. J. Rheumatol. 27(6):1562-1563.
- Bustein HJ, Janicek MJ, Skarin AT. Hypertrophic osteoarthropathy. J Clin Oncol 1997;15(7):2759-2760.