In MPS, it has been suggested that the delayed POC and SOC formation is due to altered hypertrophic differentiation resulting from persistent SOX9 expression [42,51], reduced expression of tartrate-specific acid phosphatase and matrix metalloproteinases (MMPs), and impaired osteogenic signaling through pathways, such as Wnt/β-catenin and BMP [46,47,48,49,50,51] (Figure 2). This evidence concerns the gene SOX9 and mucopolysaccharidosis.