| First Author | Kawata T | Year | 1999 |
| Journal | J Craniofac Genet Dev Biol | Volume | 19 |
| Issue | 2 | Pages | 113-7 |
| PubMed ID | 10416155 | Mgi Jnum | J:56255 |
| Mgi Id | MGI:1340652 | Citation | Kawata T, et al. (1999) Lack of the bone remodeling in osteopetrotic (op/op) mice associated with microdontia. J Craniofac Genet Dev Biol 19(2):113-7 |
| abstractText | Osteopetrosis is an inherited metabolic disease characterized by an excessive accumulation of bone. This is associated with an osteoclast deficiency. Osteopetrosis is always accompanied by the failure and/or delay of tooth eruption. The present study was conducted to examine in detail the morphological and histological changes of growth of the third molars in the osteopetrosis (op/op) mouse. At the age of 10 days, normal and op/op mice showed no detectable difference in the shape of the third molar follicles. However, the third molars in the op/op mouse became obscured by the proliferation of neighboring bone trabeculae. Moreover, no tartrate-resistant acid phosphatase-positive cells were detected on the bone surfaces of 10-day-old op/op mice. Ankylosis between the root dentin and proliferating bone trabeculae was a common feature in the 20- and 30-day-old op/op mice. The third molars erupted into the oral cavity before the age of 30 days in normal mice, and the crowns, roots, and periodontal ligaments appeared well developed. Throughout the experiment, it seemed that the primary cause of the microdontia and ankylosis of the developing root in the mutant mouse was a deficiency of osteoclasts, with attendant lack of bone remodeling. |
