Fingernails (± toenails) have increased curvature in all directions and loss of the angle between nail and nail fold (figs 3, 4). The nail fold feels boggy. The exact mechanism of clubbing is unclear; however, the platelet theory, developed in 1987, has increasing evidence behind it. Megakaryocytes are normally fragmented into platelets in the lungs, and the original theory was that any disruption to normal pulmonary circulation (inflammation, cancer, cardiac right-to-left shunting) would allow large megakaryocytes into the systemic circulation. They become lodged in the capillaries of the fingers and toes, releasing platelet-derived growth factor and vascular endothelial growth factor, both of which lead to tissue growth, vascular permeability (leading to the ‘boggy’ oedematous feel) and recruitment of inflammatory cells. This theory has been supported by necropsy evidence showing platelet microthrombi in clubbed fingers, and high levels of pdgf and vegf in patients with hypertrophic osteoarthropathy, and hypoxia may increase levels. However, this does not explain all of the changes, particularly in patients with unilateral clubbing, usually seen in neurological disorders. The jury is still out on the true pathogenesis.