Microdamage and altered vascularity at the enthesis–bone interface provides an anatomic explanation for bone involvement in the HLA–B27–associated spondylarthritides and allied disorders

Abstract

The trabecular network supporting the cortical shell is an integral part of the enthesis, transferring load to an extensive skeletal region. In many cases, tendons/ligaments are anchored directly to such networks. This functional integration is associated with microdamage and repair at the hard tissue-soft tissue interface. These findings have implications for understanding bone involvement in SpA and for the SpA concept in general, especially the hypothesis that enthesis-bone architecture may be important in disease initiation.