Another differentiating factor between type III and IV is blue sclerae; in type III, infants commonly have blue sclerae that gradually turn white with age, but blue sclerae are not commonly seen in type IV,: 294–296  although they are seen in 10% of cases.OI type III causes osteopenic bones that fracture very easily, sometimes even in utero, often leading to hundreds of fractures during a lifetime; early scoliosis that progresses until puberty; dwarfism (a final adult height frequently less than 4 feet or 120 centimetres); loose joints; and possible respiratory problems due to low rib cage volume causing low lung volumes. : 1512 Due to the severity of the issues with the bones, neurological and seizure disorders are more likely to develop in type III. : 1512  Basilar invagination, which puts pressure on the brainstem, may cause or contribute to early death; surgical treatment of it is more complex in OI cases. : 1512 : 106–107

Type IV
Collagen quantity is sufficient, but is not of a high enough quality. : 1512  Type IV is for cases of variable severity, which do not fit into either types III or I. While one of Sillences required characteristics for type IV was having normal sclerae,: 294–296 : 114  modern classification allows even those with blue sclerae to fit the criteria for type IV if they meet the other clinical requirements of the type.In type IV, bone deformity can be mild to severe, bones fracture easily (especially before puberty), dwarfism is common, vertebral collapse and scoliosis are evident, and hearing loss is possible, although uncommon.
: 168–169

Of the term
Willem Vrolik, a Dutch anatomist who was also curator of the "Museum Vrolikianum", which made him privy to many specimens of bodies having birth defects, coined the term "osteogenesis imperfecta": 683  in his bilingual Latin and Dutch language book on teratology, Illustrations of Human and Mammalian Embryogenesis, first published in 1849.Included is a description of the remains of an infant who had what is now known as perinatally fatal OI type II: 347 : 5  (as verified in a 1998 re-examination of the remains by Baljet et al.). The remains were first given to Vroliks father, who could not make sense of them. Vrolik described poorly mineralized bones, bowed long bones, and fractures in various states of healing. Vrolik correctly determined that what he termed OI in the infant was not caused by secondary rickets, but a congenital abnomality causing primary osteopenia; he theorized this was due to a lack of "intrinsic generative energy". Of its classification
Classification of OI has also evolved as scientific understanding of it has improved. Before the advent of modern genetic testing, OI was classified in two broad groups: osteogenesis imperfecta congenita, and osteogenesis imperfecta tarda, a division first proposed by the German physician E. Looser in 1906. Congenita was used to describe the modern clinical types II, III, and some cases of IV, where upon birth the condition was obvious, either due to bowing of the limbs or due to fractures sustained in utero.