The vascular origins of antero‐medial tibial bowing in congenital fibular deficiency

Abstract

Anteromedial bowing and shortening of the tibia are intrinsic features of limbs with congenital fibular deficiency (CFD). Tibial bowing occurs more frequently when the fibula is radiographically absent rather than deficient. The bowing has been attributed to rapid longitudinal growth of the tibial anlage coupled with anteromedial tibial bending moments of the posterior crural and lateral peroneal musculature unopposed in the absence of a fibular strut. Eccentric mechanical loading results in asymmetric mineral deposition and thickening of the diaphyseal cortex. Skeletogenesis depends upon an intimate interplay between the normally prefigured tibial cartilage anlage and beginning muscular contractile actions during initial vascularization of the anlage, while the embryonic limb vasculature is undergoing a series of transitions. A diaphyseal periosteal collar normally forms at the site of nutrient artery invasion and stabilizes the growing anlage. In CFD however, arteriography consistently reveals anomalous tibial nutrient arterial branches, which originate from a primitive axial artery rather than from the usual posterior tibial artery. These anomalous nutrient arteries enter the tibial shaft at the posterior aspect of the proximal metaphysis, establishing an eccentric bone collar. The developing vasculature of the embryonic limb is responsive to the then most metabolically active tissues. Disruption of the reciprocal relationship between the transitioning vasculature and the developing long bones is pivotal in producing the diverse skeletal malformations of the congenital short limb (CSL). Embryonic vascular dysgenesis contributes not only to the well‐recognized congenital tibial and fibular shortenings but also predisposes to congenital anteromedial bowing of the tibia.