Skeletal Development and Pathology in Teleost Fish

The skeleton of teleost fish serves as a dynamic framework that supports locomotion, protects vital organs and mediates mineral homeostasis. Skeletal development initiates during embryogenesis with the differentiation of mesenchymal cells into chondrocytes and osteoblasts, giving rise to cartilage and bone through endochondral and intramembranous ossification. The axial skeleton, composed of vertebral centra and associated neural and haemal arches, undergoes precise segmentation and patterning governed by conserved genetic pathways. Post-embryonic growth involves continuous remodelling, integrating osteoclastic resorption and osteoblastic deposition to accommodate increases in body size and environmental demands.

Pathological deviations in teleost skeletal development manifest as vertebral malformations—lordosis, kyphosis, scoliosis—and focal defects such as vertebral fusions or platyspondyly. These anomalies result from perturbations in genetic regulation, mineral nutrition, water chemistry, temperature and mechanical stress. In aquaculture, skeletal deformities compromise welfare, impair swimming performance and reduce market value. Conversely, naturally occurring deformities in wild populations offer insights into environmental stressors and pollutant exposure. Teleost models, notably zebrafish and gilthead seabream, have emerged as valuable systems for probing the molecular mechanisms of bone formation, mineralisation disorders and regenerative processes, with implications for human skeletal disease research.

Research from Nature Portfolio

Long-term effects of developmental temperature on gilthead seabream larvae reveal that brief exposure to lower embryonic temperatures induces a more slender body shape and enhanced swimming performance during metamorphosis. Thermal cues during the yolk-sac stage also modulate the incidence of caudal-fin abnormalities, underscoring the sensitivity of early skeletogenesis to environmental temperature.

Studies of haemal lordosis in gilthead seabream demonstrate an intrinsic capacity for skeletal remodelling during on-growing in sea cages. Nearly one third of individuals exhibiting lordotic curvature at the end of the hatchery phase revert to a normal vertebral phenotype. Morphometric analyses indicate that recovered fish are indistinguishable in body shape from those without prior deformity, revealing multi-level bone remodelling mechanisms that can restore structural integrity.

Skeletal Development and Pathology in Teleost Fish publication trend

The graph below shows the total number of articles in skeletal development and pathology in teleost fish across all publications each year (not limited to Nature Index journals).

Technical terms

Endochondral ossification: Bone formation through replacement of a cartilage template by mineralised bone.

Intramembranous ossification: Direct differentiation of mesenchymal cells into osteoblasts, leading to bone deposition without a cartilage precursor.

Haemal lordosis: A ventral curvature of the vertebral column affecting the haemal arches and associated tissues.

Osteomalacia: A condition of defective bone mineralisation resulting in softened bone and increased deformity risk.

Vertebral fusion: The pathological joining of two or more vertebral centra, impairing flexibility and function.

References

1. Long lasting effects of early temperature exposure on the swimming performance and skeleton development of metamorphosing Gilthead seabream (Sparus aurata L.) larvae. Scientific Reports (2021).
2. Recovery of haemal lordosis in Gilthead seabream (Sparus aurata L.). Scientific Reports (2019).
3. Skeletal Morphogenesis and Anomalies in Gilthead Seabream: A Comprehensive Review. International Journal of Molecular Sciences (2023).
4. Elevated Water CO2 Can Prevent Dietary-Induced Osteomalacia in Post-Smolt Atlantic Salmon (Salmo salar, L.). Biomolecules (2023).
5. Vertebral column deformity in six species of wild fish at the Coromandel coast, Bay of Bengal India. Aquaculture and Fisheries (2024).