Orthodontic movement in bone defects filled with xenogenic graft: an experimental study in minipigs.

INTRODUCTION: In this study, we investigated whether it is possible to orthodontically move a tooth into an adjacent bone defect previously filled with xenogenic grafting material, with emphasis on the reactions of the tooth roots and adjacent tissues. METHODS: Six minipigs were used. In each animal, 4 defects were created at the mesial aspects of the maxillary and mandibular first permanent molars; the defects on the right were filled with the xenograft (test side), and the opposite defects (control side) were filled with blood clots and allowed to heal spontaneously. Three months later, orthodontic appliances were placed in each quadrant to allow mesial bodily movement of the first permanent molars. When the teeth were moved about halfway into the defect spaces, the animals were killed, and the areas of interest were harvested. The mesial roots of the first molars and adjacent tissues were histologically and morphometrically evaluated. The volume density of bone tissue, the percentage of root resorption, and the bone height were evaluated with image analysis software. RESULTS: Data analysis showed that (1) the percentage of root resorption was smaller (P = .0359) for the test group (4.16%) compared with the control (6.52%); (2) there was no statistically significant differences between groups concerning the volume density of neoformed bone (P >.05); (3) the bovine bone matrix was almost totally replaced by structured bone tissue; (4) the test group had a statistically significant smaller bone height loss (2.18 mm, P = .0018) than the control group (3.26 mm). CONCLUSIONS: Based on these results, it was concluded that teeth can be moved into areas of bone defects previously filled with xenograft.

Ultrastructural morphometric analysis of ameloblasts exposed to fluoride during tooth development.

Since a considerable amount of the world population is exposed to high doses of fluoride, it is of special concern to investigate its action mechanisms during dental enamel development. In this study, the toxicity of fluoride in ameloblasts during enamel development was evaluated by means of ultrastructural morphometric analysis. A total of 18 male Wistar rats were distributed into three groups. In Group I, the animals received deionized drinking water ad libitum (negative control) and in Groups II and III, they received sodium fluorided (NaF) drinking water at doses of 7 and 100 ppm ad libitum, respectively, for 6 weeks. Morphometric data were expressed as volume density of the most significant organelles present in the secretory and maturation phases of amelogenesis such as RER, granules, lysosomes, phagic vacuoles, microfilaments and mitochondria. The results showed that the volume density of mitochondria in the 100 ppm experimental group was 29% (P < 0.05) higher than the control group in secretory ameloblasts. No remarkable differences were found in maturation ameloblasts for all organelles evaluated. Taken together, these data indicate that NaF at high doses is able to induce cellular damage in secretory ameloblasts, whereas no noxious effect was observed during maturation stage of amelogenesis as depicted by ultrastructural analysis.

Cigarette smoke affects apoptosis in rat tongue mucosa: role of bcl-2 gene family.

While it has been clearly demonstrated that smoking is the most significant exogenous factor involved in oral carcinogenesis, little is known about the global molecular and cellular changes that occur prior to the appearance of clinically detectable symptoms. Thus, the aim of this study was to investigate the expressivity of bcl-2, bax and PCNA in the rat tongue mucosa exposed to cigarette smoke by means of immunohistochemistry. A total of twelve male Wistar rats were distributed into 2 groups: negative control and experimental group exposed to cigarette smoke during 75 days. After experimental period, no histopathological changes in the tongue mucosa were detected in the negative control and the experimental group. On the other hand, an overexpression of bcl-2 was detected (p < 0.01) throughout all layers of the epithelium, whereas bax did not show significant differences (p > 0.05). Also, the labeling index for bcl-2 and bax showed an increase 75 days after cigarette exposure (p < 0.01). PCNA-labeling index did not show remarkable changes between groups. Taken together, our results show that bcl-2 is overexpressed in the rat tongue keratinocytes after cigarette smoke exposure.

Green Tea Modulates Cytokine Expression in the Periodontium and Attenuates Alveolar Bone Resorption in Type 1 Diabetic Rats.

UNLABELLED: Diabetes mellitus comprises a heterogeneous group of disorders with the main feature of hyperglycemia. Chronic hyperglycemia increases the severity of periodontal disease via an exacerbated inflammatory response, activated by advanced glycation end products and their receptor, RAGE. Therefore, anti-inflammatory agents represent potential inhibitors of this pathological interaction. In particular, green tea has been shown to possess anti-inflammatory properties mediated by its polyphenol content. OBJECTIVES: This study investigated the mechanisms by which green tea attenuates the spontaneous onset of diabetes-induced periodontitis. METHODS: Diabetes was induced in rats via a single intraperitoneal injection of streptozotocin (STZ). Diabetic and control animals were divided into water-treated and green tea-treated subgroups and were analyzed at 15, 30, 60 and 90 days after diabetes induction. Immunohistochemistry was performed to quantitatively evaluate tumor necrosis factor-α (TNF-α), receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG), interleukin-10 (IL-10) and runt-related transcription factor 2 (RUNX-2) expression in serial sections of each hemimaxilla. Morphometric measurements of the distance from the cementum-enamel junction (CEJ) of the superior distal root of the first molar to the alveolar bone crest (ABC) were performed to assess bone loss. RESULTS: Diabetes resulted in significant bone loss and alterations in the number of cells that stained positive for inflammatory mediators. In the diabetic rats treated with green tea, we observed a decreased number of cells expressing RANKL and TNF-α compared with that observed in the diabetic rats treated with water. Additionally, green tea increased the numbers of cells that stained positive for OPG, RUNX-2 and IL-10 in the diabetic rats. CONCLUSION: Green tea intake reduces expression of the pro-inflammatory cytokine TNF-α and the osteoclastogenic mediator RANKL to normal levels while increasing expression of the anti-inflammatory cytokine IL-10, the osteogenesis-related factor RUNX-2 and the anti-osteoclastogenic factor OPG. Therefore, green tea represents a potential therapeutic agent for the treatment of diabetes-related periodontal disease.