The presence of skeletal anomalies in farmed teleost fish is currently a major problem in aquaculture, entailing economical, biological and ethical issues. The common occurrence of skeletal abnormalities in farmed fish and the absence of effective solutions for avoiding their onset or definitely culling out the affected individuals as early as possible from the productive cycle, highlight the need to improve our knowledge on the basic processes regulating fish skeletogenesis and skeletal tissues differentiation, modelling and remodelling. Severe skeletal anomalies may actually occur throughout the entire life cycle of fish, but their development often begins with slight aberrations of the internal elements. Comprehensive investigation efforts conducted on reared larvae and juveniles could provide a great contribution in filling the gap in knowledge, as skeletogenesis and skeletal tissue differentiation occur during these early life stages. The aim of this review is to provide a synthetic but comprehensive picture of the actual knowledge on the ontogeny, typologies and occurrence of skeletal anomalies, and on the proposed causative factors for their onset in larvae and juveniles of European farmed fish. The state‐of‐art of knowledge of these issues is analysed critically intending to individualize the main gaps of knowledge that require to be filled, in order to optimize the morphological quality of farmed juveniles.

This critical review summarizes the knowledge about fish skeletal tissues and inherent normal and anomalous development. Particular emphasis is given to existing literature on reared European fishes. The aim was to identify the main gaps of knowledge that require to be filled, in order to precociously identify anomalous developmental patterns that lead to skeletal anomalies in reared finfish larvae and juveniles. The review also aims to extend our knowledge about the factors that are possibly involved in the onset of skeletal anomalies. The final goal is the optimization of the morphological quality of farmed juvenile fish.

The return of Atlantic salmon (Salmon salar) to their home river for spawning coincides with drastic skeletal alterations in both sexes. Most prominent is the development of a kype (hook) at the tip of the lower jaw in males. Salmon that survive spawning have to cope with the kype throughout their life, unless it disappears after spawning, as was suggested in the early literature. To understand the fate of the kype skeleton, we compared morphological and histological features of kypes from pre‐spawned mature anadromous males (grilse) with post‐spawned males (kelts). The kype of male grilse is supported by fast‐growing skeletal needles that differ from regular dentary bone. In kelts, growth of the kype skeleton has stopped and skeletal needles are resorbed apically by osteoclasts. Simultaneously, and despite the critical physiological condition of the animals, proximal parts of the kype skeleton are remodelled and converted into regular dentary bone. Apical resorption of the skeleton explains reports of a decrease of the kype in kelts. The conversion of basal kype skeleton into regular dentary bone contributes to the elongation of the dentary and probably also to the development of a larger kype in repetitive spawning males.

Over the last years the zebrafish imposed itself as a powerful model to study skeletal diseases, but a limit to its use is the poor characterization of collagen type I, the most abundant protein in bone and skin. In tetrapods collagen type I is a trimer mainly composed of two α1 chains and one α2 chain, encoded by COL1A1 and COL1A2 genes, respectively. In contrast, in zebrafish three type I collagen genes exist, col1a1a, col1a1b and col1a2 coding for α1(I), α3(I) and α2(I) chains. During embryonic and larval development the three collagen type I genes showed a similar spatio-temporal expression pattern, indicating their co-regulation and interdependence at these stages. In both embryonic and adult tissues, the presence of the three α(I) chains was demonstrated, although in embryos α1(I) was present in two distinct glycosylated states, suggesting a developmental-specific collagen composition. Even though in adult bone, skin and scales equal amounts of α1(I), α3(I) and α2(I) chains are present, the presented data suggest a tissue-specific stoichiometry and/or post-translational modification status for collagen type I. In conclusion, this data will be useful to properly interpret results and insights gained from zebrafish models of skeletal diseases.