COL1A2 and osteogenesis imperfecta: Substitutions in the type I procollagen C-propeptide cleavage site in COL1A1 or COL1A2 were first reported with a mild dominant OI phenotype in patients with normal or increased DXA z-score and bone mineralization increased higher than in classical OI on BMDD, and impaired C-propeptide processing [32, 33].