The arterial supply of the lesser metatarsal heads: a vascular injection study in human cadavers.

The possibility of avascular changes of the metatarsal heads following forefoot surgery has been previously documented. The aim of this study was to investigate the arterial supply of the lesser metatarsal heads with regard to osteotomies of these bones. We used epoxy resin injections and a modified Spalteholz technique in human cadaveric specimens to demonstrate the intraosseous and extraosseous blood supply of the lesser metatarsals. The metatarsal heads had two arterial sources: 1. The dorsal metatarsal arteries, which arose from the dorsalis pedis artery, and 2. The plantar metatarsal arteries, which are branches of the posterior tibial artery. These two vessels typically anastomosed at two sites about the metatarsal heads, forming a vascular ring and provided an extensive extraosseous arterial network around the metatarsal heads. Small arterial branches of this network run distally on the metatarsal cortex to enter the bone of the metatarsal head. The nutrient arteries traversed the cortex of the metaphysis close to the capsular and ligamentous insertions to provide multiple branches for the supply of the subchondral bone. Extensive capsular stripping during metatarsal head osteotomies results in damage to the medial and lateral head vessels.

The role of vasculature and angiogenesis for the pathogenesis of degenerative tendons disease.

More than 100 years ago Wilhelm Roux (1895) introduced the term "functional adaptation to anatomy and physiology". Compared with other organ systems the functional adaptation processes are best identifiable in the locomotor system, like for example in the two types of tendons: traction and gliding tendons. Traction tendons are tendons where the direction of pull is in line with the direction of the muscle (e.g. Achilles tendon). Gliding tendons (e.g. tibialis posterior tendon) change direction by turning around a bony or fibrous hypomochlion. In this region the tendon is subjected to intermittent compressive and shear forces and the extracellular matrix consists of avascular fibrocartilage. Avascularity is considered to be a key factor for the etiology of degenerative tendon disease. The repair capability after repetitive microtrauma is strongly compromised in avascular tissue of gliding tendons. Reduced vascularity is not a specific feature of gliding tendons; several studies have shown that the number and size of blood vessels are largely shortened in the waist of the Achilles tendon. However, histological biopsies from degenerated Achilles tendons and Doppler flow examinations revealed a high blood vessel density in patients with degenerative tendon disease. Angiogenesis is mediated by angiogenic factors and recent studies have shown that the vascular endothelial growth factor (VEGF) is highly expressed in degenerative Achilles tendons, whereas VEGF expression is nearly completely downregulated in healthy tendons. Several factors are able to upregulate VEGF expression in tenocytes: hypoxia, inflammatory cytokines and mechanical load. Since VEGF has the potential to stimulate the expression of matrix metalloproteinases and inhibit the expression of tissue inhibitors of matrix metalloproteinases tissue inhibitor of metalloproteinases (TIMP) in various cell types (e.g. endothelial cells, fibroblasts, chondrocytes), this cytokine might play a significant role for the pathogenetic processes during degenerative tendon disease. An animal experiment in the rabbit has shown that local injection of VEGF reduced the material properties of the Achilles tendon. These experimental findings are in accordance with clinical results that a locally administered (in the area with neovascularization) sclerosing drug (Polidocanol) has a beneficial effect on chronic mid-portion Achilles tendinosis. In conclusion, decreased and increased vascularity might be involved in the pathogenesis of degenerative Achilles tendon disease.