The temporomandibular joint (TMJ) showed characteristic anatomy and functions contrast to the other joints. In particular, children or young adolescent with the progressive temporomandibular disorder (TMD) showed remarkable changes in their mandibular growth and occlusion. The purpose of this study was to elucidate the functional and biomechanical causes for the maxillofacial deformities of TMD. A typocranial experiment was performed using a plastic skull model by simulating the mandibular movement after condylectomy. The directional forces of masticatory and suprahyoid muscles were reproduced on the typocranial skull model by elastics connecting between mandible and adjacent bony structures. Resultantly, the mandible of unilaterally or bilaterally condylectomized mandible was rotated downward and backward by the activation of masticatory and suprahyoid muscles. When unilaterally or bilaterally condylectomized mandible was activated by masticatory, suprahyoid and perioral muscles, the mandible was less rotated downward and backward than the cases activated by masticatory and suprahyoid muscles only. In the typocranial experiment after unilateral condylectomy the mandible was rapidly deviated toward the affected side, but this deviation was much reduced when the mandible was intensely supported by perioral muscles. By the compensatory response against the overload of TMJ due to the mandible body resection the typocranial experiment also produced the deepening of antegonial notch by the increased force of mylohyoid and perioral muscles. These findings suggest that after condylectomy the posterior fibers of mylohyoid and perioral muscles become hypertrophic and induce the characteristic mandibular deformities, i.e., deepening of antegonial notch and bowing of posterior ramus, which are similar to the mandibular changes in the progressive TMD.

Osteoarthrosis in TMJ is known to accompany characteristic features of the craniofacial malformation and malocclusion. In order to explain the mechanism that brings about the typical mandibular changes relating to the frequent clinical symptom, i.e., the limited mouth opening in TMJ patients. The present study investigated the mandibular morphology of the rabbit, also intentional TMJ osteoarthrosis was performed on the TMJ of the rabbits and their morphological changes were observed. A total of 12 New Zealand house rabbits weighing an average of 3 kgwere used and all left side joints were surgically meniscectomized and right side joints were used as controls. The rabbits were sacrificed in one week, two weeks, one month, three months and 5 months after the menisectomy, and the removed TMJs were examined by histological and radiographical methods and analyzed statistically. It was found that the mandibular morphology caused by osteoarthritis in the TMJ was characterized by the decrease in size of the ascending ramus, posterior ramus bowing, deep antegonial notch and thickening of the cortex in inferior and posterior borders of the mandible, that the similar features were also observed in the rabbit mandible. When the menisectomy was performed in the unilateral side of rabbit TMJ, the mandibular changes including the increased depth of antegonial notch and posterior ramus bowing occurred only on the affected side. These data suggested that the limitation of the mandibular movement and altered masticatory pattern by meniscectomy affects the structural remodeling of the mandible and TMJ likely the TMJ osteoarthrosis

As pulp calcification occurs at least fifty percent of total teeth, the focal calcification in pulp chamber usually appears in all age groups. However, the pulp calcification is one of the important pathologic changes affecting the pulp vitality. In order to elucidate the mechanism of pulp calcification during the retrogressive degeneration of pulp tissue we performed an immunohistochemical study for proteases (MMP-3, MMP-10, and cathepsin-G), antiproteases (TIMP-1, α1- AT) and proteins involving tissue protection (TGase-2 and HSP-70). In the normal pulp tissue MMP-3 and MMP-10 were weakly expressed, but cathepsin-G and TIMP-1 were rarely expressed. Around the calcifying tissue of MMP-3, MMP- 10, and α1-AT were predominant, but TIMP-1 and cathepsin-G were sparsely expressed. On the other hands, TGase-2 and HSP-70 were condensed in the proximal fibrous tissue. These data suggest that the pulp calcification is related to retrogressive pulp degeneration, which could be resulted in the incomplete digestion of the degenerated stromal tissue by different proteases. We presume that the aberrant protease digestion of chronic pulpal pathosis, i.e., sclerotic fibrosis, chronic pulp degeneration, etc., may enhance the dystrophic calcification in dental pulp.

Normal development of human fetal teeth during prenatal period play an important role in analyzing abnormal teeth formation and examining pathologic approach to abnormal teeth formation. The purposes of this study were to describe the normal development of dental hard tissues in fetal teeth compared to abnormal teeth formation through review and literature. We will apply these study to examine the pathologic alterations of human teeth in the future.

The primary growth center (MdPGC) of human fetal mandible was conspicuously distinguished in the soft X-ray view of fetal mandibles.1) As the peripheral adaptive growth of mandible advanced during the postnatal period, the MdPGC became overshadowed by condensed cortical bone. However, in the well-processed radiograms of adult mandible a condensed radiopaque image, measuring 0.5-1.0 cm in diameter, can be observed below the apex of first premolar. In this study we aimed to trace a sclerotic sequela of mandibular primary growth center during postnatal period. Panoramic radiograms of two hundreds adults and soft X-ray views of thirty dry mandible were analyzed by statistical methods. The adult MdPGC was clearly distinguishable from the mental foramen. The area of MdPGC was seldom changed in the older persons, even in the edentulous mandibles. Additionally, the benign lesions of odontogenic cysts and tumors hardly destroyed the original structure of MdPGC, while the malignant tumors of squamous cell carcinoma and metastatic cancer rapidly destroyed and resolved the radiopaque area of the MdPGC.