Effects of transverse bodily movements of maxillary premolars on the surrounding hard tissue.

INTRODUCTION: This experimental study was designed to (1) produce buccal translation of maxillary premolars and (2) evaluate the effects on the buccal alveolar bone. METHODS: A randomized split-mouth study was designed based on 7 adult male beagle dogs. The experimental side received a custom cantilever appliance fabricated to produce a translatory force through the maxillary second premolar's center of resistance. The contralateral second premolar received no appliance and served as the control. The premolars underwent 6-7 weeks of buccal translation, followed by 3 weeks of fixed retention. Biweekly tooth movements were evaluated using intraoral and radiographic measurements. Pretreatment and posttreatment models were measured to assess tipping. Three-dimensional microscopic tomography was used to quantify the amount and density of buccal bone. Bone formation and turnover were assessed using fluorescent labeling, hematoxylin and eosin staining, tartrate-resistant acid phosphatase staining, and bone sialoprotein immunostaining. RESULTS: The applied force (100 g of force) translated (1.4 mm) and minimally tipped (4°) the experimental teeth. Lateral translation produced dehiscences at the mesial and distal roots, with 2.0 mm and 2.2 mm loss of vertical bone height, respectively. Bone thickness decreased significantly (P < 0.05) at the apical (∼0.4 mm), midroot (∼0.4 mm), and coronal (∼0.2 mm) levels. Fluorescent imaging, hematoxylin and eosin staining, and immunostaining for bone sialoprotein all showed new bone formation extending along the entire periosteal surface of the second premolar's buccal plate. Tartrate-resistant acid phosphatase staining demonstrated greater osteoclastic activity on the experimental than that of control sections. CONCLUSIONS: New buccal bone forms on the periosteal surface during and after tooth translation, but the amount of bone that forms is less than the amount of bone loss, resulting in a net decrease in buccal bone thickness and a loss of crestal bone.

Gender differences in the growing, abnormal, and aging jaw.

Despite wide variations in the size and shape of the human face, head, and body, there is remarkable consistency for quantifiable gender-specific facial traits. The relationships between the growing jaws and tooth eruption are complex, but they show gender-specific trajectories in children and adolescents. Disturbances in genetic, endocrine, and nutritional regulatory controls result in gender-specific and nonspecific disorders. Gender-specific differences are also apparent in the aging jaw, with the acceleration of jawbone atrophy upon loss of teeth, especially in women.

Regulation of cell surface protease matriptase by HAI2 is essential for placental development, neural tube closure and embryonic survival in mice.

Hypomorphic mutations in the human SPINT2 gene cause a broad spectrum of abnormalities in organogenesis, including organ and digit duplications, atresia, fistulas, hypertelorism, cleft palate and hamartoma. SPINT2 encodes the transmembrane serine protease inhibitor HAI2 (placental bikunin), and the severe developmental effects of decreased HAI2 activity can be hypothesized to be a consequence of excess pericellular proteolytic activity. Indeed, we show here that HAI2 is a potent regulator of protease-guided cellular responses, including motogenic activity and transepithelial resistance of epithelial monolayers. Furthermore, we show that inhibition of the transmembrane serine protease matriptase (encoded by St14) is an essential function of HAI2 during tissue morphogenesis. Genetic inactivation of the mouse Spint2 gene led to defects in neural tube closure, abnormal placental labyrinth development associated with loss of epithelial cell polarity, and embryonic demise. Developmental defects observed in HAI2-deficient mice were caused by unregulated matriptase activity, as both placental development and embryonic survival in HAI2-deficient embryos were completely restored by the simultaneous genetic inactivation of matriptase. However, neural tube defects were detected in HAI2-deficient mice even in the absence of matriptase, although at lower frequency, indicating that the inhibition of additional serine protease(s) by HAI2 is required to complete neural development. Finally, by genetic complementation analysis, we uncovered a unique and complex functional interaction between HAI2 and the related HAI1 in the regulation of matriptase activity during development. This study indicates that unregulated matriptase-dependent cell surface proteolysis can cause a diverse array of abnormalities in mammalian development.