Hypertrophic Pulmonary Osteoarthropathy (HPOA) is described as bilateral, symmetric periosteal new bone formation, synovial effusions, and clubbing of the digits. The bone changes are seen in the distal extremities and begins as a low grade inflammatory process in the periosteum followed by new bone formation. Multiple layers of new bone are deposited which results in cortical thickening that can be seen on plain film. The diametaphysis of the tibia, fibula, radius, and ulna are usually involved. Other bony involvement includes the scapula which has been noted to be involved in two-thirds of the known cases, clavicles, ribs, and pelvic bones. The abnormalities are more obvious in the lower than upper extremities and again, in the bones distal to the knees and elbows rather than in the femurs and humeri.

Although these findings may be present on plain film, bone scan is the more sensitive modality. The bone scan findings are symmetric, diffusely increased uptake along the cortical margins of the diaphysis and metaphysis of the distal extremities. This is consistent with periosteal new bone formation. Also, the periarticular regions may be involved and increased due to the associated synovitis.

Clinically, the periosteal involvement in the distal extremities may produce a burning or deep-seated aching pain. Pain can be described as incapacitating.

Two types of hypertrophic osteoarthropathy are present.
There is a primary variant that is rare and thought to be congenital;however, the secondary form is acquired and associated with multiple disease processes. (see Table)

Pulmonary
- various neoplasms including carcinoma
- sarcoidosis
- various lung infections
- cystic fibrosis
- interstitial pneumonitis

Cardiovascular
- valvular disease
- cyanotic congenital heart disease
- infected valves or grafts
- aneurysms

Gastrointestinal
- neoplasms
- inflammatory bowel disease
- sprue

Thyroid
- Graves' disease - thryoid acropachy


Hypertrophic Pulmonary Osteoarthropathy (HPOA)occurs in 5-10% of patients with intrathoracic malignancies (ie, bronchogenic carcinoma, pleural tumors, and less frequently lung metastasis). Many theories of HPOA have been developed. The latest consideration mentions the role of platelets and associated growth factors triggered by endothelial cells. Megakaryocytes and large platelet particles get fragmented in the passage through the diseased lung. These fragments interact with endothelial cells that trigger the release of growth factors causing proliferation of connective tissue and periosteum.