INTRODUCTIONrnThe vertebrate skeleton has evolved as a dynamic system that serves numerous functions, such as protecting internal organs, creating attachment sites for muscles to produce locomotion, providing a reservoir for minerals, and serving as a hematopoietic niche. Many signaling pathways control the patterning, growth and maturation of skeletal structures from early development to adulthood.1rnThe vertebrate bony skeleton is formed through two processes, intramembranous ossification or endochondral ossification (EO),1–2 the latter of which is responsible for long bone development. EO is initiated in the fetus and continues postnatally in the growth plates (GP) until growth cessation in adolescence.2–3 The rate of longitudinal bone growth is determined by the rate of chondrocyte proliferation, the size of the hypertrophic chondro-cytes, and cartilage degradation and replacement by bone. Chondrocytes in different zones of the GP are distinguished by their differentiation stage, morphology and matrix production. In the proliferative zone (PZ), chondrocytes are arranged in long-itudinal columns, where they rapidly proliferate and deposit typical cartilage extracellular matrix (ECM) components, especially collagen type 2 (Col2) and aggrecan (Acan). Next, chondrocytes exit the cell cycle and become prehypertrophic by expressing the type X collagen (Col10) and Indian hedgehog (Ihh) genes. Prehypertrophic chondrocytes increase in size to become hypertrophic cells.1,4 In the hypertrophic zone (HZ), cells become enlarged, swollen and vacuolated and are characterized by secretion of Col10, alkaline phosphatase, and angiogenic factors.