Osteopetrosis is an inherited metabolic disease characterized by an excessi
ve accumulation of bone. This is associated with an osteoclast deficiency.
Osteopetrosis is always accompanied by the failure and/or delay of tooth er
uption. The present study was conducted to examine in detail the morphologi
cal and histological changes of growth of the third molars in the osteopetr
osis (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, t
he third molars in the op/op mouse became obscured by the proliferation of
neighboring bone trabeculae. Moreover, no tartrate-resistant acid phosphata
se-positive cells were detected on the bone surfaces of 10-day-old op/op mi
ce. 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 er
upted into the oral cavity before the age of 30 days in normal mice, and th
e crowns, roots, and periodontal ligaments appeared well developed. Through
out 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 o
steoclasts, with attendant lack of bone remodeling.