Meeting Abstract
Bone is a tough tissue, subjected to repetitive and cyclic loading throughout life. In the absence of proper adaptation to changes in loads, bones will be destined to fail due to damage accumulation. To avoid failure, bone-forming cells (osteoblasts) and bone-resorbing cells (osteoclasts) are continuously reshaping (model) and repairing (remodel) bone material. The main orchestrators of these synergetic processes are osteocytes, which constitute more than 90% of all bone cells. Considering the pivotal role of osteocytes , it is surprising that while bones of all vertebrates, including basal fish, contain a huge network of osteocytes, the bones of most extant fish completely lack them (anosteocytic bones). This raises questions regarding the ability of anosteocytic bones to adapt to loads or to regulate adaptation. We show remarkable response of anosteocytic bones to loading, such as osteoblast recruitment and architectural changes. Despite the lack of osteocytes, we detected expression of the main modeling-regulating gene, SOST (normally expressed exclusively by osteocytes), in peripheral cells such as osteoblasts and chondrocytes. Macro-to-nano structural and mechanical studies revealed similarity of adaptive response in both osteocytic and anosteocytic fish bones. To our surprise, not only is the adaptive response similar, but osteocytic bones of basal fish also express SOST by their peripheral cells – similarly to what we found in anosteocytic bones. Our findings suggest a novel form of modeling-control in fish bones, which differs from that of other vertebrate groups and might explain the evolutionary shift toward anosteocytic skeleton in fish.
