Among the genetic mouse models of OA described,[7] mutations in major developmental regulatory genes typically required conditional knockouts due to embryonic lethality (i.e. HH).[13] Mutations in ECM proteins like COL2A1 display a variety of congenital malformations of the skeleton mirroring human pedigrees of patients with chondrodysplasias.[7] There are lines of mice that develop osteoarthritis spontaneously (SRT/Ort), but it is noted that this is not typical of human disease.[31] Del1 KO mice develop more severe OA than WT after an inciting trauma. Here, COL2A1 is linked to chondrodysplasia.