The separation of type V from type IV OI, its clinical type, was initially suggested even before its genetic cause was known, by Glorieux et al. in 2000. Type V is relatively common compared to other genetically defined types of OI—4% of OI patients at the genetics department of the Brazilian Hospital de Clínicas de Porto Alegre were found to have it. Type VI – With the same clinical features as type III, it is distinguished by bones which have an appearance similar to that seen in osteomalacia. : 168  Type VI is caused by a loss-of-function mutation in the SERPINF1 gene on chromosome 17p13.3. : 170 
Type VII – OI caused by a mutation in the gene CRTAP on chromosome 3p22.3; clinically similar to OI types II and III, depending on affected individual. Type VII was the first recessive OI type confirmed, initially found among First Nations people in Quebec. Type VIII – OI caused by a mutation in the gene LEPRE1 on chromosome 1p34.2; clinically similar to OI types II and III, depending on affected individual. Type IX – OI caused by homozygous or compound heterozygous mutation in the PPIB gene on chromosome 15q22.31. Type X – OI caused by homozygous mutation in the SERPINH1 gene on chromosome 11q13. Type XI – OI caused by mutations in FKBP10 on chromosome 17q21. The mutations cause a decrease in secretion of trimeric procollagen molecules. Other mutations in this gene can cause autosomal recessive Bruck syndrome, which is similar to OI.
In the rare cases of infants who survive their first year of life, severe developmental and motor delays are seen; neither of two infants studied in 2019, both aged around two years, had achieved head control, and both required a ventilator to breathe.Type II is also known as the "lethal perinatal" form of OI, and is not compatible with survival into adulthood. Due to similarly severely deformed bones, sometimes infants with severe type III are wrongly initially classified as type II; once long-term survival is shown, they are considered as having type III instead. : 1511

Type III
Collagen quantity is sufficient, but is not of a high enough quality. : 1512  Clinical differentiation between types III and IV is not always simple, and is further confounded by the fact that an untreated adult with type IV may have worse symptoms than a treated adult with type III;: 1511  features only found in type III are its progressively deforming nature: 1511–1512  and the presence of a face with a "triangular" appearance.