Pathogenesis of secondary hypertrophic osteoarthropathy: a hypothesis

Abstract

Wide ranges both in the location and the pathological state of the primary disease associated with hypertrophic osteoarthropathy (HO) have been noted. The combined distribution of the glossopharyngeal and vagus nerves appears to coincide with the range of locations of the primary disease associated with HO. These two nerves are believed to contribute to the innervation of the blood vessels in this same area. This hypothesis states that: i) some of this innervation is part of a blood volume control system; and ii) by an inappropriate stimulation of this system, as a result of blood-flow in an anomalous vascular rearrangement lying close to the primary disease associated with HO, a cerebral salt centre is stimulated to retain extra-cellular sodium. A secondary atrial natriuretic peptide over-secretion ensues and a "near steady-state" is established, with the presence of excess fluid and dilated vessels in all four limbs. Thus, the pathogenesis of HO and the distribution of an extra-renal volume control system are reciprocal facets of the same question.