An in-depth examination of the Crtap−/− murine model of OI revealed a series of periodontal dysfunction including decreased alveolar bone volume and mineral density, increased PDL space, ectopic calcification within the PDL, bone-tooth ankylosis, altered immunostaining of extracellular matrix proteins in bone and PDL, increased pSMAD5, and more numerous osteoclasts on alveolar bone surfaces. This evidence concerns the gene CRTAP and tooth ankylosis.