OI affects people of all races and has been reported in all continents. OI is the most common cause of hereditary childhood bone fragility, with the overall prevalence of OI estimated to be between 1 in 10,000 to 1 in 20,000 live births.[4]Marini JC, Forlino A, Bächinger HP, et al. Osteogenesis imperfecta. Nat Rev Dis Primers. 2017 Aug 18;3:17052.
http://www.ncbi.nlm.nih.gov/pubmed/28820180?tool=bestpractice.com
Approximately 25,000 individuals in the US are thought to be affected by OI.[5]Pillion JP, Vernick D, Shapiro J. Hearing loss in osteogenesis imperfecta: characteristics and treatment considerations. Genet Res Int. 2011;2011:983942.
https://www.hindawi.com/journals/gri/2011/983942
http://www.ncbi.nlm.nih.gov/pubmed/22567374?tool=bestpractice.com
However, these figures are likely to be underestimates as people with the milder forms of OI may go unrecognised.[6]Oheim R, Tsourdi E, Seefried L, et al. Genetic diagnostics in routine osteological assessment of adult low bone mass disorders. J Clin Endocrinol Metab. 2022 Jun 16;107(7):e3048-57.
https://academic.oup.com/jcem/article/107/7/e3048/6547251
http://www.ncbi.nlm.nih.gov/pubmed/35276006?tool=bestpractice.com
[7]Robinson ME, Rauch F. Mendelian bone fragility disorders. Bone. 2019 Sep;126:11-7.
http://www.ncbi.nlm.nih.gov/pubmed/31039433?tool=bestpractice.com
With the rapid discovery of new genes that cause OI, genetic classification comprising more than 20 types has been defined.[4]Marini JC, Forlino A, Bächinger HP, et al. Osteogenesis imperfecta. Nat Rev Dis Primers. 2017 Aug 18;3:17052.
http://www.ncbi.nlm.nih.gov/pubmed/28820180?tool=bestpractice.com
COL1A1 and COL1A2-related OI, which are transmitted as autosomal dominant disorders and include OI types I, II, III, and IV, account for up to 90% of all cases of OI, while the remaining subtypes are rare.[8]Patel RM, Nagamani SC, Cuthbertson D, et al. A cross-sectional multicenter study of osteogenesis imperfecta in North America - results from the linked clinical research centers. Clin Genet. 2015 Feb;87(2):133-40.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5529599
http://www.ncbi.nlm.nih.gov/pubmed/24754836?tool=bestpractice.com
[9]El-Gazzar A, Högler W. Mechanisms of bone fragility: from osteogenesis imperfecta to secondary osteoporosis. Int J Mol Sci. 2021 Jan 10;22(2):625.
https://www.doi.org/10.3390/ijms22020625
http://www.ncbi.nlm.nih.gov/pubmed/33435159?tool=bestpractice.com
[10]Byers PH, Wallis GA, Willing MC. Osteogenesis imperfecta: translation of mutation to phenotype. J Med Genet. 1991 Jul;28(7):433-42.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1016951
http://www.ncbi.nlm.nih.gov/pubmed/1895312?tool=bestpractice.com
See Classification.
Some of the rare autosomal recessively transmitted forms of OI occur at a higher frequency in certain populations due to founder variants, i.e., variants that were present in a single ancestor or small number of ancestors from which the population arose (e.g., OI type VII [CRTAP; First Nations in Ontario, Canada], OI type VIII [P3H1; West Africa], and OI type XI [FKBP10; Turkey]).[11]Marini JC, Dang Do AN. Osteogenesis imperfecta. In: Feingold KR, Anawalt B, Blackman MR, et al, eds. Endotext [Internet]. South Dartmouth, MA: MDText.com, Inc; 2020 Jul 26.
https://www.ncbi.nlm.nih.gov/books/NBK279109
http://www.ncbi.nlm.nih.gov/pubmed/25905334?tool=bestpractice.com