下顎体部後方に発現する小骨欠損 (So-called Stafne's bone cavity) の形成経過ならびに成因に関する考察

抄録

In 1942, Stafne reported bone cavity of radiolucent lesion below the mandibular canal in the region between the foward part of the mandibular angle and the third molar. The cavity appears either round or oval, and the walls of the cavity are generally dense and thick.
Other cases of this type of cavity or defect have been reported by many author after Stafne's article. Considering the etiology, it has been suggested that the cavity or defect may be caused by embryonic abnormality, anomalies of developmental, pulsation of the artery and pressure of hypertrophied submandibular gland. Because of the uncertain etiology, various terms have been proposed to designate the condition, such as Stafne's bone cavity, latent bone cyst, static bone cabity or defect, mandibular embryonic defect, idiopathic bone cavity, developmental bone defect.
Although many cases have been reported, the course of the developmental of bone defect is not yet recorded. We examined the developmental process of this kind of defect.
A case was soon in a 43-year-old male patient. His dentist found lower right first molar cementoma in a radiograph and referred him to us for treatment. On this occasion, nothing remarkable was found except first molar from the panoramic investigation. Three years later, a new radiograph revealed that a small area of bone rarefaction (radiolucent 20 × 15 mm) had appeared in the region of mandibular canal between trigonum retromolare and distal root of the third molar. 10 months later, the radiolucent area moved downward to the inferior border of the mandibular canal. It was turned into an oval shape and outlined by a radiopaque border. After another 6 months, the oval area showed a definite shape that was surround by a compact bone.
The latest radiographic examination was performed after another year and no change was detected (10 × 5 mm). On microscopic examination, the lesion consisted of fibrous connective tissue with neurovascular structure. The arteries revealed thrombosis with recanalization of the thrombus and bursting hemorrhage. The wall of the defect consisted of compact bone without osteoblast or osteoclast.
We considered that the defect was a bone destruction caused by hemorrhage by rhexis of the thrombosed small arteries in the mandibular canal and that the typical defect of cortex outline could be a result from failure of bone repair owing to the persistent existence of the soft tissue in the bone defect.