Joint Program in Nuclear Medicine

Secondary Hypertrophic Osteoarthropathy

Kavitha Vadde, MD
J. Stevan Nagel, MD

October 5, 1999

Presentation

A 67 year old white male presented with fevers and bilateral lower extremity edema for 3 weeks. Chest radiograph is notable for an 8 cm mass in the left upper lung (shown by arrows) that is confirmed on CT of the chest (mass shown by arrows). CT guided fine needle aspiration of the lung mass revealed non-small cell carcinoma of the lung.

Imaging Findings

Bone Scintigraphy

A Tc-99m MDP bone scan was performed to assess for skeletal metastases. The Tc-99m MDP bone scan shows prominent lobulated cortical uptake of the radiotracer in the distal upper and lower extremities, most marked in the tibias and fibulas (shown by arrows).

Plain Radiographs

Correlative radiographs of the right knee and left knee reveal mild periosteal reaction along the diaphysis and metaphysis of the distal femur and proximal tibia.

Diagnosis

Hypertrophic osteoarthropathy secondary to non-small cell lung carcinoma

Discussion

Hypertrophic osteoarthropathy (HOA) is a syndrome characterized by proliferative changes in the skin and skeleton. Proliferative periostitis of the long bones, oligopolysinovitis, and digital clubbing are commonly seen. Two forms of the syndrome are seen,

a rare idiopathic from called pachydermoperiostitis, and
the more common secondary form.

Secondary hypertrophic osteoarthropathy was initially described in association with chronic suppurative infection and malignancy of the lung and pleura. The first case report of hypertrophic osteoarthropathy associated with an intrathoracic tumor was published in 1933 by Schiassi (1). Hypertrophic osteoarthropathy has since been documented in association with numerous disease processes, including cardiovascular, hepatobiliary, gastrointestinal, and endocrine disorders.

The pathogenesis of hypertrophic osteoarthropathy remains unclear. The syndrome typically affects the distal aspects of the extremities and progresses centrally. It can manifest in a localized form in association with right to left shunts, where the extremity preferentially receiving the shunted blood is affected. A current theory proposes that hypertrophic osteoarthropathy is secondary to faulty pulmonary clearance of macrothrombocytes that lodge in distal capillary beds and release growth factors leading to acropachy (2).

Bone Scintigraphy in Hypertrophic Osteoarthropathy

Bone scintigraphy is a very sensitive in detecting hypertrophic osteoarthropathy. Scintigraphic detection of new bone formation precedes radiographic detection. Scintigraphic findings characteristic of hypertrophic osteoarthropathy include symmetric increased uptake along the cortical margins of the diaphyses of long bones (parallel tract or double stripe sign). Increased juxtaarticular uptake and distal phalangeal uptake is seen due to synovitis and clubbing respectively. The primary radiographic manifestation of hypertrophic osteoarthropathy is periosteal reaction that increases in extent and thickness with increasing duration of disease (3, 4).

Ali et al (5) studied the distribution of skeletal involvement in hypertrophic osteoarthropathy. In their series of 48 cases, the limbs were always involved. The tibia and fibula were the most commonly affected bones. Either or both was involved in all cases. The second most common sites of involvement were the femurs, and the hands. The most common sites of involvement in the central skeleton were the mandible and scapula. A symmetric and regular pattern of cortical tracer uptake was seen along the periosteum of long bones in approximately 80%. Disease activity was greater in the lower extremities compared to the upper extremities in 98%.

Differentiation of Hypertrophic Osteoarthropathy and Metastatic Disease

The pattern of distribution of hypertrophic osteoarthropathy distinguishes it form skeletal metastases. In metastatic disease the axial skeleton (vertebrae and ribs) and the medullary cavity of long bones rather than the cortices are commonly affected. The clinical, scintigraphic and radiographic findings remit with treatment of the underlying disorder in secondary hypertrophic osteoarthropathy. Recurrence of the primary disease is often associated with recurrence of hypertrophic osteoarthropathy.

References

1. Carcassi U. History of hypertrophic osteoarthropathy (HOA). Cln Exp Rheumatol (1992 May-June) 10 Suppl 7:3-7.

2. Martinez-Lavin M. Pathogenesis of hypertrophic osteoarthropathy. Clin Exp Rheumatol (1992 May-June) 10 Suppl 7.

3. Rosenthal, et al. Observations on radionuclide imaging in hypertrophic pulmonary osteoarthropathy. Radiology (1976 August) 120:359-362.

4. Pineda CJ et al. Periositis in hypertrophic osteoarthropathy: relationship to disease duration. AJR ( 1987 Apr) 148(4)773-8.

5. Ali A et al. Distribution of hypertrophic pulmonary osteoarthropathy. AJR (1980 Apr) 134(4): 771-80.

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J. Anthony Parker, MD PhD, Tony_Parker@CareGroup.Harvard.edu