Bone turnover rates can be altered by metabolic and mechanical demands. Due to the difference in the pattern of loading, we hypothesized that there are differences in bone remodeling rates between the maxillary and mandibular alveolar processes. Furthermore, in a canine model, the alveolar process of teeth that lack contact (e.g., second premolars) would have a different turnover rate than bone supporting teeth with functional contact (e.g., first molars). Six skeletally mature male dogs were given a pair of calcein labels. After sacrifice, specimens representing the anterior and posterior locations of both jaws were prepared for examination by histomorphometric methods to evaluate the bone volume/total volume (BV/ TV; %), bone volume (mm 2 ), mineral apposition rate (MAR; mm/day), and bone formation rate (BFR; %/year) in the alveolar process. There were no significant differences (P > 0.05) in the BV/TV within the jaws. The bone volume within the alveolar process of the mandible was 2.8-fold greater than in the maxilla. The MAR was not significantly different between the jaws and anteroposterior locations. However, the BFR was significantly (P < 0.0001) greater in the mandible than in the maxilla. The anterior location had higher (P ¼ 0.002) remodeling than the posterior location in the maxilla but not in the mandible. While there was a greater bone mass and increased remodeling in the mandible, no remodeling gradient in the coronal-apical direction was apparent in the alveolar process. Bone adaptation probably involves a complex interplay of bone turnover, mass, and architecture.

Cyclooxygenase-2 (COX-2) and the prostaglandin products generated as a result of COX-2 activity mediate a variety of biological and pathological processes. Scarless healing occurs in fetal skin in the first and second trimesters of development. This scarless healing process is known to proceed without a significant inflammatory response, which appears to be important for the lack of scarring. Because the COX-2 pathway is an integral component of inflammation, we investigated its role in the fetal repair process using a mouse model of scarless fetal wound healing. COX-2 expression in scarless and fibrotic fetal wounds was examined. In addition, the ability of exogenous prostaglandin E(2) to alter scarless fetal healing was evaluated. The results suggest that the COX-2 pathway is involved in scar production in fetal skin and that targeting COX-2 may be useful for limiting scar formation in adult skin.

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One mechanism of bone adaptation is alteration in tissue level material properties. We hypothesized that alteration in the indentation modulus of the alveolar process is an adaptive response to the localized mechanical environment. Forty-eight specimens representing anterior and posterior regions of the maxilla and mandible were obtained from 6 mature male beagle dogs. The indentation properties of the alveolar bone proper and more distant osteonal cortical bone were estimated. The bone types were further divided into 3 regions (coronal, middle, and apical), with 27 indents being made in each region of tooth-supporting bone. There was a significant difference (p < 0.001) in the indentation moduli of the jaws (maxilla/mandible), location (anterior/posterior), and bone type (alveolar bone proper vs. cortical bone). However, statistical interactions exist which preclude the simple interpretation of results. The distribution of relative stiffness provides a better understanding of bone adaptations in the alveolar process.

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