Rat Maxilla Research Articles

Microdamage in the alveolar process of rat maxillae after orthodontic tooth movement.

Playing a decisive role in bone remodeling, microdamage was recently associated with orthodontic tooth movement in pigs. The present study was conducted to evaluate microdamage and its potential association with orthodontic tooth movement in the alveolar process of rat maxillae. The upper right molars of 24 male Wistar rats (10 weeks old) were splinted and loaded against the (likewise splinted) upper incisors with 25 cN using a Nitinol coil spring. Four groups of 6 animals were treated in this fashion for 1, 2, 4, or 7 days. The upper left quadrants served as controls. The maxillae were halved, gently prepared, and stained en bloc with basic fuchsin. After embedding in resin, 80-μm-thick parasagittal sections were ground parallel to the mesial root of the first molar. These were used to assess microdamage under transmitted and epifluorescent light, also counting and measuring the length of microcracks. Differences between the loaded and unloaded side and between mesial and distal were checked using a Wilcoxon test and were considered significant at ≤ 0.05. Microdamage (in the form of diffuse damage and microcracks) was observed in both the loaded and control jaw halves, as well as on the mesial and distal sides in all four groups. Microcracks averaged 30-100 μm in length and 0.3-1.7/mm(2) in density. While they were more prevalent in the loaded than the control jaw halves, this difference was not statistically significant. The alveolar process of rat maxillae is characterized by microdamage (in the form of microcracks and diffuse damage) regardless of whether and for how long orthodontic loading has taken place. Within the limitations of this experimental study, our results do not confirm previous findings of significantly higher prevalence on the pressure side on the first day after initiating orthodontic tooth movement.

Osteoprotegerin Expressed by Osteoclasts

Osteoprotegerin (OPG) is secreted by stromal and osteoblastic lineage cells and inhibits osteoclastogenesis by preventing the interaction of receptor activator of nuclear factor-κB ligand (RANKL) with receptor activator of nuclear factor-κB (RANK). In this study, the expression of OPG in osteoclasts themselves and its biological functions during osteoclastogenesis were investigated for the first time. OPG expression in vivo in the developing rat maxilla was examined by immunofluorescence analysis. OPG expression in osteoclasts during in vitro osteoclastogenesis was determined by reverse-transcription polymerase chain-reaction (RT-PCR), Western blot, and immunofluorescence staining. We determined the function of OPG produced by osteoclasts during osteoclastogenesis by silencing the OPG gene. The effects of OPG on bone-resorbing activity and apoptosis of mature osteoclasts were examined by the assay of resorptive pit formation on calcium-phosphate-coated plate and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining, respectively. In the immunofluorescence findings, strong immunoreactivities were unexpectedly seen in multinucleated tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts around the growing and erupting tooth germs in the rat alveolar bone. In vitro, OPG expression was significantly increased during the differentiation of osteoclasts from mouse bone-marrow-derived cells treated with a combination of macrophage colony-stimulating factor (M-CSF) and RANKL. Interestingly, it was found that OPG small interfering (si)RNA treatment during osteoclastogenesis enhanced the sizes of osteoclasts, but attenuated their bone-resorbing activity. Also, the increased chromosomal DNA fragmentation and caspase-3 activity in the late phase of osteoclastogenesis were found to be decreased by treatment with OPG siRNA. Furthermore, effects of OPG siRNA treatment on osteoclastogenesis and bone-resorbing activity were recovered by the treatment of exogenous OPG. These results suggest that OPG, expressed by the osteoclasts themselves, may play an auto-regulatory role in the late phase of osteoclastogenesis through the induction of apoptosis.

Effects of alendronate on the peri-implant bone in rats.

The purpose of this study was to determine the effects of alendronate on the peri-implant bone in rat maxillae with the aid of micro-computed tomographic, histologic, and biochemical analyses. Thirty-six male Sprague-Dawley rats were used. After extraction of the maxillary first molars, each rat was given periodic subcutaneous injections of either alendronate (alendronate group) or saline (control group). Customized implants were placed bilaterally 4weeks after these injections. The rats were sacrificed at either 4, 8, or 12weeks after implantation (4-, 8-, and 12-week groups, respectively; n=6 rats per group). Microcomputed tomographic and histologic analyses were conducted for all rats. Biochemical analyses were performed at four time points for the 12-week groups. There were no significant differences between the groups on microcomputed tomographic and histologic analyses. All of the measured biochemical parameters tended to decrease over time, with significant differences among some time points within each group. The serum osteocalcin level was significantly lower in the 12-week alendronate group than in the control group (P<0.05). Three approaches were utilized in evaluating the effects of alendronate. It appears serum osteocalcin levels may serve as an adjuvant marker for this purpose, although further studies are required to confirm this.

Mechanical induction of interleukin-11 regulates osteoblastic/cementoblastic differentiation of human periodontal ligament stem/progenitor cells.

The periodontal ligament (PDL) is continually exposed to mechanical loading caused by mastication or occlusion. Physiological loading is thus considered a key regulator of PDL tissue homeostasis; however, it remains unclear how this occurs. We recently reported that an appropriate magnitude of mechanical stretch can maintain PDL tissue homeostasis via the renin-angiotensin system. In the present study, we investigated the expression of interleukin-11 (IL-11) in human primary PDL cells (HPDLCs) exposed to stretch loading, the contribution of angiotensin II (Ang II) to this event and the effects of IL-11 on osteoblastic/cementoblastic differentiation of human PDL progenitor cells (cell line 1-17). Human primary PDL cells, derived from human tissues, with or without antagonists against the Ang II receptors AT1 or AT2, were subjected to cyclical stretch loading with 8% elongation for 1h. Expression of IL-11 was measured by ELISA in these cultures and by immunohistochemistry in the sectioned maxillae of rats. The osteoblastic/cementoblastic potential of cell line 1-17 was determined using cell proliferation, gene expression and Alizarin Red staining. Positive staining for IL-11 was observed in the PDL of rat maxillae and in cultures of HPDLCs. In HPDLCs exposed to stretch, expression of the IL11 gene and the IL-11 protein were up-regulated, concomitant with an increase in Ang II and via AT2. Recombinant human IL-11 (rhIL-11) stimulated an increase in expression of mRNA for the cementoblast-specific marker, CP-23, and for the osteoblastic markers, osteopontin and bone sialoprotein, and promoted proliferation in cell line 1-17. In addition, rhIL-11 also increased the degree of mineralized nodule formation in cell line 1-17 cultures treated with CaCl2 . Mechanical loading appears to control proliferation and osteoblastic/cementoblastic differentiation of human PDL stem/progenitor cells through the regulation of Ang II and AT2 by IL-11.

Accelerated Tooth Movement and Temporary Skeletal Anchorage Devices (TSADs).

Accelerated Tooth Movement and Temporary Skeletal Anchorage Devices (TSADs).

A Novel Rat Model of Orthodontic Tooth Movement Using Temporary Skeletal Anchorage Devices: 3D Finite Element Analysis and In Vivo Validation.

The aim of this animal study was to develop a model of orthodontic tooth movement using a microimplant as a TSAD in rodents. A finite element model of the TSAD in alveolar bone was built using μCT images of rat maxilla to determine the von Mises stresses and displacement in the alveolar bone surrounding the TSAD. For in vivo validation of the FE model, Sprague-Dawley rats (n = 25) were used and a Stryker 1.2 × 3 mm microimplant was inserted in the right maxilla and used to protract the right first permanent molar using a NiTi closed coil spring. Tooth movement measurements were taken at baseline, 4 and 8 weeks. At 8 weeks, animals were euthanized and tissues were analyzed by histology and EPMA. FE modeling showed maximum von Mises stress of 45 Mpa near the apex of TSAD but the average von Mises stress was under 25 Mpa. Appreciable tooth movement of 0.62 ± 0.04 mm at 4 weeks and 1.99 ± 0.14 mm at 8 weeks was obtained. Histological and EPMA results demonstrated no active bone remodeling around the TSAD at 8 weeks depicting good secondary stability. This study provided evidence that protracted tooth movement is achieved in small animals using TSADs.

Virtual tissue alignment and cutting plane definition – a new method to obtain optimal longitudinal histological sections

Histomorphometric evaluation of the buccal aspects of periodontal tissues in rodents requires reproducible alignment of maxillae and highly precise sections containing central sections of buccal roots; this is a cumbersome and technically sensitive process due to the small specimen size. The aim of the present report is to describe and analyze a method to transfer virtual sections of micro-computer tomographic (CT)-generated image stacks to the microtome for undecalcified histological processing and to describe the anatomy of the periodontium in rat molars. A total of 84 undecalcified sections of all buccal roots of seven untreated rats was analyzed. The accuracy of section coordinate transfer from virtual micro-CT slice to the histological slice, right-left side differences and the measurement error for linear and angular measurements on micro-CT and on histological micrographs were calculated using the Bland-Altman method, interclass correlation coefficient and the method of moments estimator. Also, manual alignment of the micro-CT-scanned rat maxilla was compared with multiplanar computer-reconstructed alignment. The supra alveolar rat anatomy is rather similar to human anatomy, whereas the alveolar bone is of compact type and the keratinized gingival epithelium bends apical to join the junctional epithelium. The high methodological standardization presented herein ensures retrieval of histological slices with excellent display of anatomical microstructures, in a reproducible manner, minimizes random errors, and thereby may contribute to the reduction of number of animals needed.

Sequential Platelet-Derived Growth Factor–Simvastatin Release Promotes Dentoalveolar Regeneration

Timely augmentation of the physiological events of dentoalveolar repair is a prerequisite for the optimization of the outcome of regeneration. This study aimed to develop a treatment strategy to promote dentoalveolar regeneration by the combined delivery of the early mitogenic factor platelet-derived growth factor (PDGF) and the late osteogenic differentiation factor simvastatin. By using the coaxial electrohydrodynamic atomization technique, PDGF and simvastatin were encapsulated in a double-walled poly(D,L-lactide) and poly(D,L-lactide-co-glycolide) (PDLLA-PLGA) microspheres in five different modes: microspheres encapsulating bovine serum albumin (BB), PDGF alone (XP), simvastatin alone (SB), PDGF-in-core and simvastatin-in-shell (PS), and simvastatin-in-core and PDGF-in-shell (SP). The microspheres were characterized using scanning electronic microscopy, and the in vitro release profile was evaluated. Microspheres were delivered to fill large osteotomy sites on rat maxillae for 14 and 28 days, and the outcome of regeneration was evaluated by microcomputed tomography and histological assessments. Uniform 20-μm controlled release microspheres were successfully fabricated. Parallel PDGF-simvastatin release was noted in the PS group, and the fast release of PDGF followed by the slow release of simvastatin was noted in the SP group. The promotion of osteogenesis was observed in XP, PS, and SP groups at day 14, whereas the SP group demonstrated the greatest bone fill, trabecular numbers, and thickest trabeculae. Bone bridging was evident in the PS and SP group, with significantly increased osteoblasts in the SP group, and osteoclastic cell recruitment was promoted in all bioactive molecule-treated groups. At day 28, osteogenesis was promoted in all bioactive molecule-treated groups. Initial corticalization was noted in the XP, PS, and SP groups. Osteoblasts appeared to be decreased in all groups, and significantly, a greater osteoclastic cell recruitment was noted in the SB and SP groups. Both PDGF and simvastatin facilitate dentoalveolar regeneration, and sequential PDGF-simvastatin release (SP group) further accelerated the regeneration process through the enhancement of osteoblastogenesis and the promotion of bone maturation.

Simvastatin inhibits lipopolysaccharide‐induced osteoclastogenesis and reduces alveolar bone loss in experimental periodontal disease

Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase and have anti-inflammatory effects independent of cholesterol lowering. Recent clinical studies have indicated that statin intake has a beneficial effect on periodontal disease. However, the underlying mechanisms have not been well understood. In the current study, we employed a rat model with lipopolysaccharide (LPS)-induced periodontal disease and determined the effect of simvastatin, a commonly prescribed statin, on osteoclastogenesis, gingival inflammation and alveolar bone loss. Sprague-Dawley rats were injected with Aggregatibacter actinomycetemcomitans LPS in periodontal tissue three times per week for 8 wk and part of the rats with LPS injection were also given simvastatin via gavage. After the treatments, the rat maxillae were scanned by microcomputed tomography and the images were analyzed to determine alveolar bone loss. To explore the underlying mechanisms, the effect of simvastatin on osteoclastogenesis and gingival expression of proinflammatory cytokines were also determined by tartrate-resistant acid phosphatase staining and real-time polymerase chain reaction assays, respectively. Results showed that LPS treatment markedly increased bone loss, but administration of simvastatin significantly alleviated the bone loss. Results also showed that LPS treatment stimulated osteoclastogenesis and the expression of inflammatory cytokines, but simvastatin significantly modulates the stimulatory effect of LPS on osteoclastogenesis and cytokine expression. This study demonstrated that simvastatin treatment inhibits LPS-induced osteoclastogenesis and gingival inflammation and reduces alveolar bone loss, indicating that the intake of simvastatin may hinder the progression of periodontal disease.

Dual delivery of PDGF and simvastatin to accelerate periodontal regeneration in vivo

The emphasis on periodontal regeneration has been shifted towards the harmonization of bioactive molecules and physiological phases during regeneration. This study investigated whether the combination and sequential-release of platelet-derived growth factor (PDGF, mitogen) and simvastatin (differentiation factor) facilitated periodontal regeneration. PDGF and simvastatin were encapsulated in double-walled poly-( d,l-lactide) and poly-(d,l-lactide-co-glycolide) (PDLLA-PLGA) microspheres using the co-axial electrohydrodynamic atomization technique. Critical-sized periodontal defects on rat maxillae were filled with microspheres encapsulating BSA-in-core-shell (BB), PDGF-in-shell (XP), simvastatin-in-core and BSA-in-shell (SB), simvastatin-in-core and PDGF-in-shell, or unfilled with microspheres (XX), and examined at 14 and 28 days post-operatively. The resultant microspheres were around 15 μm diameter with distinct core–shell structure, and the fast-release of PDGF followed by slow-release of simvastatin was noted in the SP group. The SP group demonstrated significantly greater bone volume fraction and decreased trabecular separation compared to the XX group at day 14, and milder inflammatory cells infiltration and elevated tartrate-resistant acid phosphatase level were noted at day 28. Fibers were also well-aligned and obliquely inserted onto the root surface similar to native periodontal ligament with signs of cementogenesis in the SP group. In conclusion, the combination and sequential-release of PDGF-simvastatin accelerates the regeneration of the periodontal apparatus.

Effect of cyclical forces on the periodontal ligament and alveolar bone remodeling during orthodontic tooth movement

To investigate the effect of externally applied cyclical (vibratory) forces on the rate of tooth movement, the structural integrity of the periodontal ligament, and alveolar bone remodeling. Twenty-six female Sprague-Dawley rats (7 weeks old) were divided into four groups: CTRL (unloaded), VBO (molars receiving a vibratory stimulus only), TMO (molars receiving an orthodontic spring only), and TMO+VB (molars receiving an orthodontic spring and the additional vibratory stimulus). In TMO and TMO+VB groups, the rat first molars were moved mesially for 2 weeks using Nickel-Titanium coil spring delivering 25 g of force. In VBO and TMO+VB groups, cyclical forces at 0.4 N and 30 Hz were applied occlusally twice a week for 10 minutes. Microfocus X-ray computed tomography analysis and tooth movement measurements were performed on the dissected rat maxillae. Tartrate-resistant acid phosphatase staining and collagen fiber assessment were performed on histological sections. Cyclical forces significantly inhibited the amount of tooth movement. Histological analysis showed marked disorganization of the collagen fibril structure of the periodontal ligament during tooth movement. Tooth movement caused a significant increase in osteoclast parameters on the compression side of alveolar bone and a significant decrease in bone volume fraction in the molar region compared to controls. Tooth movement was significantly inhibited by application of cyclical forces.

Relationships between oral infections and blood glucose concentrations or HbA1c levels in normal and diabetic rats

To measure glycosylated haemoglobin (HbA1c) in a diabetic model as a means of investigating apical periodontitis and periodontal disease for their effects on both blood glucose concentrations and long-term glycaemic control. Wistar rats (n=80) were assigned to one of eight groups (10 animals/group): control (G1), apical periodontitis (G2), periodontal disease (G3), apical periodontitis and periodontal disease (G4), diabetic (G5), diabetic with apical periodontitis (G6), diabetic with periodontal disease (G7) and diabetic with apical periodontitis and periodontal disease (G8). A diabetic state was induced with streptozotocin. Apical periodontitis was induced by dental exposure to the oral environment. Periodontal disease was induced by periodontal ligature. Blood glucose concentrations were measured at 0, 6, 30 and 60days. After euthanization, rat maxillae were excised and processed for histopathology and for measurement of HbA1c levels by ion exchange chromatography. Data were tabulated and subject to statistical analysis (P<0.05). The inflammatory infiltrate and alveolar bone resorption were more severe in diabetic rats (P<0.05). Diabetic rats exhibited higher levels of HbA1c independent of apical periodontitis or periodontal disease (P<0.05). However, the presence of oral infections in diabetic rats was associated with increased blood glucose concentrations (P<0.05). Oral infections affect glycaemic conditions in diabetic rats and increase HbA1c levels in normoglycaemic or diabetic rats.

Soft diet causes greater alveolar osteopenia in the mandible than in the maxilla

ObjectiveTo investigate changes in the bony microstructure of the upper and lower alveolar bone during masticatory loading induced by soft diet feeding in growing rats. DesignThree-week-old male Wistar rats were randomly divided into two groups. Rats were fed with either pellets [control group (n=6)] or a soft diet [experimental group (n=6)] for nine weeks. 3D-microstructure of the alveolar bone of the first molar region (M1) was examined by micro-CT analysis. ResultsMicro-CT images showed increased marrow spaces of the inter-radicular alveolar bone around the rat mandibular M1 in the experimental group compared with that in the control group. The bone volume/tissue volume ratio, trabecular thickness, trabecular number, mean intercept length, trabecular width and trabecular star volume for the mandibular M1 inter-radicular alveolar bone were lower in the experimental group than in the control group. Marrow space star volume was increased in the experimental group compared with the control group. ConclusionsThese results suggest that alveolar osteopenia is more extensive in the mandible than the maxilla in rats that experience low masticatory loading during growth.

Controlling the Proliferation and Differentiation Stages to Initiate Periodontal Regeneration

The success of periodontal regeneration depends on the coordination of early cell proliferation and late cell differentiation. The aim of this study was to investigate whether the proliferation or differentiation stage predominantly promotes the initiation of periodontal regeneration. Critical-sized periodontal defects were surgically created on rat maxillae and filled with poly-(d,l-lactide-co-glycolide)–poly-d,l-lactide hybrid microspheres encapsulating platelet-derived growth factor (PDGF, a promoter of mitogenesis), simvastatin (a promoter of osteogenic differentiation), or bovine serum albumin (a control). The encapsulation efficiency and in vitro release profiles of the microspheres were determined by high-performance liquid chromatography and enzyme-linked immunosorbent assay. The maxillae were harvested after 10 or 14 days and assessed by micro-computed tomography, histology, and immunohistochemistry for regeneration efficacy and cell viability. The rapid release of PDGF was observed within the first week, whereas a slow release profile was noted for simvastatin. The PDGF-treated specimens demonstrated a significantly higher bone volume fraction compared with bovine serum albumin– (p < 0.05) or simvastatin-treated (p < 0.05) specimens at day 14. Histologically, active bone formation originating from the defect borders was noted in both the PDGF- and the simvastatin-treated specimens, and functionally aligned periodontal ligament fiber insertion was only observed in the PDGF-treated specimens. The significant promotion of mitogenesis by PDGF treatment was also noted at day 14 (p < 0.05). In conclusion, increased mitogenesis or osteogenic differentiation may stimulate osteogenesis, and the upregulation of mitogenesis by PDGF appears to play a role in the initiation of periodontal regeneration.

Osteoimmunological mechanisms involved in orthodontically and bacterially induced periodontal stress

Orthodontic tooth movement is known to cause sterile inflammation of the periodontal ligament (PDL). It may also be accompanied by pathological effects of external apical root resorption, with interindividual differences in the incidence and extent of resorption. An involvement of autoimmunological mechanisms is currently under discussion. This study aimed to improve our understanding of similarities between the inflammatory mechanisms underlying the pathophysiology of periodontitis and root resorption. Human PDL cells were stimulated with interleukin (IL)-1β/IL-17A/IFN-γ, or left non-stimulated. Their potential for phagocytosis was then evaluated by incubation with dextran or E. coli or S. aureus particles, followed by flow cytometric and immunohistochemical analysis. Real-time polymerase chain reaction (PCR) was used to analyze receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) expression in PDL cells. Verification was obtained in vivo by studying IL-17A, RANKL, and OPG expression in biopsies of inflamed periodontal tissues and in biopsies of rat maxillae with mechanically induced root resorption. Statistical analysis included Wilcoxon's rank sum test to analyze gene expression data and one-way ANOVA in conjunction with Tukey's post hoc test to analyze flow cytometric data. PDL cells phagocytosed foreign particles under both inflammatory and non-inflammatory conditions. Furthermore, IL-17A significantly downregulated RANKL expression while significantly upregulating OPG expression in PDL cells. These immunomodulatory cytokines were also demonstrable in both inflammatorily altered periodontal tissues and root resorption lacunae, while the incidence of IL-7A was strikingly variable in resorption areas. PDL cells were demonstrated to effect phagocytosis and to express immunomodulatory molecules, which proves their capability of participating in periodontal osteoimmunological processes. The development of root resorption and periodontitis appears to be governed by similar pathophysiological mechanisms.

PDGF-Simvastatin Delivery Stimulates Osteogenesis in Heat-induced Osteonecrosis

Heat generated during implant osteotomy might lead to osteonecrosis and delayed bone repair, thus resulting in impaired early osseointegration and fixation of bone-anchoring devices. In this study, we proposed to overcome heat-induced injury to bone by fabricating core-shell polymeric biodegradable microspheres encapsulating a mitogenic factor, platelet-derived growth factor (PDGF), and a differentiation factor, simvastatin, in a simultaneous or sequential release profile. Microspheres encapsulating bovine serum albumin (BSA), PDGF, simvastatin, PDGF-in-core with simvastatin-in-shell, and simvastatin-in-core with PDGF-in-shell were delivered to fill standardized osteotomy sites on edentulous ridges of rat maxillae under irrigated or non-irrigated conditions. In the absence of irrigation, significant reduction of cell viability and increase in inflammation and sequestrum formation without evidence of osteogenesis were observed. Both PDGF and simvastatin deliveries facilitated cell viability and reduced osteonecrosis. Localized osteogenesis was seen under simvastatin treatment, while generalized but primitive osteogenesis was noted in PDGF-treated osteotomy sites. In addition, sequential PDGF-simvastatin delivery further augmented osteogenesis and promoted bone maturation. The results suggested that sequential PDGF-simvastatin delivery was an effective modality to prevent heat-induced complications and facilitate bone apposition after implant osteotomy, potentially favoring the early fixation of bone-anchoring devices and oral implant osseointegration.

Brachytherapy-Mediated Bone Damage in a Rat Model Investigating Maxillary Osteoradionecrosis

To assess clinical and radiologic findings from targeted radiotherapy to the rat maxilla and to compare findings with a recently developed rat model of mandibular osteoradionecrosis (ORN). A prospective, controlled animal study. Ten male Sprague-Dawley rats were divided into an experimental group receiving catheter-assisted high-dose-rate brachytherapy (n=6) and a control group with catheter-assisted sham therapy (n=4). The second left maxillary molar was extracted 1 week after radiation, and the maxilla was harvested 3 weeks after dental extraction. We used a standardized method with micro-computed tomography to determine the ratio of bone volume to total volume of the dental extraction socket. On the gross clinical examination, all rats had mucosal coverage of the dental extraction site, whereas only the brachytherapy group demonstrated scarring of the mucosa. The median bone volume to total volume was 0.21 for the brachytherapy group and 0.49 for the control group (P=.01). Similar to the mandible, the maxilla is susceptible to radiogenic bone injury as demonstrated by the significant decrease in bone volume of the radiated dental extraction socket. Despite radiologic similarities to mandibular ORN in the rat model, the maxilla demonstrated a more benign clinical course with a complete absence of bone exposure. Differences in the maxillary bone and microenvironment of the maxilla compared with the mandible may explain the subclinical response to radiation and lower incidence of maxillary ORN seen in patients. This maxillary model can be combined with our high-dose-rate mandibular ORN model to investigate these differences and better understand ORN.

Enhanced alveolar bone loss in a model of non‐invasive periodontitis in rice rats

The rice rat (Oryzomys palustris) develops periodontitis-like lesions when fed a diet rich in sucrose and casein (H-SC). We aimed to establish whether this model can accurately mimic the development of human periodontitis. For this purpose, 28-day-old rice rats (15/group) were assigned to standard (STD) or H-SC diets and sacrificed after 6, 12, and 18 weeks. Jaws were processed for morphometric, histometric, histologic, histomorphometric, and micro-CT analyses. We found a progressive increase in horizontal alveolar bone loss (ABL) with age in maxillae of rats fed the STD diet as determined by morphometry. The H-SC diet exacerbated horizontal ABL at the palatal surface at 12 and 18 weeks. Furthermore, increased vertical ABL was detected in mandibles and maxillae of rats fed the H-SC diet for 12 and/or 18 weeks by histometry and micro-CT. Remarkably, the H-SC diet significantly increased bone remodeling at the interproximal alveolar bone of mandibles from rats fed for 6 weeks, but not in those fed for longer periods. These findings indicate that the H-SC diet induced a transient increase in alveolar bone remodeling, which is followed by ABL characteristic of moderate periodontitis.

Hard tissue formation induced by synthetic oligopeptide derived from an enamel matrix derivative

Background: Eosinophilic round bodies (ERBs) are composed of fragments of amino acid sequences of varying lengths, which represent a portion of exon 5 of amelogenin gene. ERBs have previously been shown to accumulate in the backs of rats subcutaneously injected with the product Emdogain®. In the present study, an oligopeptide with an amino acid sequence similar to this portion was artificially synthesized, and its effects were examined. Methods: The peptide solution was applied to periodontal defects created on the maxillae of rats. Sections from these tissues were histopathologically and immunohistochemically examined at 7 and 14 days after the start of the experiment. Results: In the experimental group, hard tissue had formed on the surface of exposed dentin, and both osteopontin and collagen type I (COLI) were localized around the hard tissue. The hard tissue was stained with periodic acid-Schiff (PAS) more deeply than was the dentin, and the fibers that were positive for COLI were vertically inserted in the rim of the newly-formed hard tissue. No hard tissue formation was found in the control group. Conclusion: These results suggest that synthetic oligopeptide administration can induc

Experimental Craniofacial Composite Tissue Allotransplantation (CCTA) Models in Rats

Rats are the most frequently used animals in composite tissue allotransplantation (CTA) studies and most craniofacial composite tissue transplantation models are described in rats. During the last 10 years, a total of 8 different craniofacial composite tissue allotransplantation (CCTA) models have designed and developed in rats. These models include full face/scalp transplants, hemiface transplants, composite hemiface/calvarium transplants, rat maxilla allotransplants, composite osteomusculocutaneous hemiface/mandible/tongue flap transplants, composite midface allotransplants, total osteocutaneous hemifacial allotransplantation model and composite face and eyeball allotransplant model with optic nerve. All these models provide a basic and scientific foundation for future success in CTA in the clinical setting. This review presents different experimental models of CCTA in rats which are relevant to observed in clinical scenario cases of severe facial deformities.