Resonance frequency analysis of long-term implant success in the posterior partially edentulous mandible.

OBJECTIVE: Resonance frequency analysis (RFA) has enabled the assessment of implant stability in terms of implant stability quotient (ISQ) units. This study evaluated the long-term stability of endosseous implants according to an ISQ scale of 1 to 100, as estimated by RFA in the posterior partially edentulous mandible. METHOD AND MATERIALS: A 2-stage procedure was used to place 328 Braäemark implants in the edentulous mandibular molar region (second premolar to second molar) of 113 patients (49 men and 64 women). Patients were followed at regular intervals postoperatively, and ISQ scores were evaluated by RFA every year for 10 years. RESULTS: The implant success rate was 100%. ISQ scores did not significantly differ in the pattern of stability changes among different bone quantities and qualities during long-term follow-up. There was no significant difference in implant stability among the mandibular sides, the sites, and the sexes. CONCLUSION: Long-term stability of Bränemark implants was excellent in the posterior partially edentulous mandible.

Immunohistochemical detection of phosphorylated Akt, PI3K, and PTEN in ameloblastic tumors.

OBJECTIVE: To evaluate roles of the Akt signaling pathway in oncogenesis and cytodifferentiation of odontogenic tumors, expression of phosphorylated Akt (pAkt), PI3K, and PTEN was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: 11 tooth germs, 40 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with antibodies against pAkt, PI3K, and PTEN. RESULTS: Immunoreactivity for pAkt, PI3K, and PTEN was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and ameloblastic tumors. The levels of immunoreactivity for pAkt and PI3K were slightly higher in ameloblastic tumors than in tooth germs. Plexiform ameloblastomas showed significantly higher expression of PI3K than follicular ameloblastomas, and PI3K immunoreactivity in ameloblastomas without cellular variation was significantly higher than that in acanthomatous ameloblastomas. The level of PTEN immunoreactivity was significantly lower in ameloblastomas than in tooth germs. CONCLUSION: Expression of pAkt, PI3K, and PTEN in tooth germs and ameloblastic tumors suggests that these signaling molecules regulate cell survival and growth in normal and neoplastic odontogenic tissues by mediating growth factor signals. Increased expression of pAkt and PI3K and decreased expression of PTEN in ameloblastic tumors may participate in oncogenesis of odontogenic epithelium by activating the Akt signaling pathway.

Immunohistochemical detection of platelet-derived endothelial cell growth factor/thymidine phosphorylase and angiopoietins in ameloblastic tumors.

BACKGROUND: To evaluate the roles of angiogenic factors in the development and progression of odontogenic tumors, expression of platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) and of angiopoietins in ameloblastic tumors as well as in tooth germs. METHODS: Tissue specimens of 11 tooth germs, 44 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against PD-ECGF/TP and angiopoietin-1 and -2. RESULTS: Immunohistochemical reactivity for PD-ECGF/TP was detected in mesenchymal cells in tooth germs and stromal cells in ameloblastic tumors, and the level of immunoreactivity for PD-ECGF/TP was significantly higher in ameloblastomas than in tooth germs. Granular cell ameloblastomas showed PD-ECGF/TP reactivity in granular neoplastic cells as well as in stromal cells. Immunoreactivity for angiopoietin-1 and -2 was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and in benign and malignant ameloblastic tumors. Malignant ameloblastic tumors had decreased angiopoietin-1 reactivity and ameloblastic carcinomas had increased angiopoietin-2 reactivity as compared with the respective levels in tooth germs and ameloblastomas. Immunohistochemical reactivity for angiopoietin-2 was slightly higher in follicular ameloblastomas than in plexiform ameloblastomas. CONCLUSION: Expression of PD-ECGF/TP and angiopoietin-1 and -2 in tooth germs and ameloblastic tumors suggests that these angiogenic factors participate in tooth development and odontogenic tumor progression by regulating angiogenesis. Altered expression of PD-ECGF/TP and angiopoietins in ameloblastic tumors may be involved in oncogenesis, malignant potential, and tumor cell differentiation.

Immunohistochemical detection of retinoblastoma protein and E2 promoter-binding factor-1 in ameloblastomas.

BACKGROUND: To clarify the roles of cell cycle regulation in oncogenesis and cytodifferentiation of odontogenic tumors, expression of retinoblastoma protein (RB) and E2 promoter-binding factor-1 (E2F-1) was analyzed in ameloblastomas as well as in tooth germs. METHODS: Tissue specimens of 10 tooth germs, 40 benign ameloblastomas, and five malignant ameloblastomas were examined immunohistochemically with the use of antibodies against RB, E2F-1, and phosphorylated RB. Ki-67 antigen immunostaining was made as a marker of cell proliferation. RESULTS: Immunohistochemical reactivity for RB, E2F-1, phosphorylated RB, and Ki-67 was detected in the nuclei of odontogenic epithelial cells near the basement membrane in tooth germs and benign and malignant ameloblastomas. The number of cells positive for phosphorylated RB was nearly equal to or slightly less than the number of cells positive for RB or E2F-1. The number of Ki-67-positive cells was slightly more than the numbers of cell positive for RB, E2F-1, or phosphorylated RB. The levels of immunoreactivity for RB, E2F-1, phosphorylated RB, and Ki-67 were slightly higher in benign and malignant ameloblastomas than in tooth germs. Plexiform ameloblastomas showed significantly higher expression of RB than follicular ameloblastomas. Ki-67 immunoreactivity was significantly higher in ameloblastic carcinomas than in metastasizing ameloblastomas. CONCLUSION: Similar immunoreactivity for RB, E2F-1, phosphorylated RB, and Ki-67 in tooth germs and ameloblastomas indicated cellular expression of phosphorylated RB and active-free E2F-1 in both normal and neoplastic odontogenic tissues. Expression of RB, E2F-1, and phosphorylated RB was considered to be involved in cell proliferation and differentiation of odontogenic epithelium via control of the cell cycle.

Detection of mitochondria-mediated apoptosis signaling molecules in ameloblastomas.

BACKGROUND: To investigate the roles of the apoptosis signaling pathway mediated by mitochondria in oncogenesis and cytodifferentiation of odontogenic tumors, expression of pathway signaling molecules was analyzed in ameloblastomas as well as in tooth germs. METHODS: Tissue specimens of 12 tooth germs, 41 benign ameloblastomas, and five malignant ameloblastomas were examined by reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry to determine the expression of cytochrome c, apoptotic protease-activating factor-1 (APAF-1), caspase-9, and apoptosis-inducing factor (AIF). RESULTS: The mRNA expression of APAF-1, caspase-9, and AIF was detected in all samples of normal and neoplastic odontogenic tissues. Immunohistochemical reactivity for cytochrome c, APAF-1, caspase-9, and AIF was detected in both normal and neoplastic odontogenic tissues. Expression of cytochrome c and AIF was evident in odontogenic epithelial cells neighboring the basement membrane, and APAF-1 and caspase-9 were detected in most odontogenic epithelial cells. Immunoreactivity for cytochrome c in tooth germs was slightly weaker than that in benign and malignant ameloblastomas. Keratinizing cells in acanthomatous ameloblastomas and granular cells in granular cell ameloblastomas showed a decrease or loss of immunoreactivity for these mitochondria-mediated apoptosis signaling molecules. Expression of AIF was obviously low in ameloblastic carcinomas. CONCLUSION: Expression of cytochrome c, APAF-1, caspase-9, and AIF in tooth germs and ameloblastomas suggests that the mitochondria-mediated apoptotic pathway has a role in apoptotic cell death of normal and neoplastic odontogenic epithelium. Expression of these mitochondrial apoptosis signaling molecules might be involved in oncogenesis, cytodifferentiation, and malignant transformation of odontogenic epithelium.

Histomorphometric study of the stability of newly formed bone after elevation of the floor of the maxillary sinus.

We studied the remodelling process of newly formed bone and the distribution of osteoclasts in the augmented space after elevation of the floor of the maxillary sinus in rabbits. Histologically, 10 weeks after grafting, there was some newly formed lamellar bone embedded in fatty tissue. Histomorphometric analysis showed that the augmented height and augmented area decreased significantly from 2 to 6 weeks. The number of osteoclasts on newly formed bone, adjacent to the elevated sinus membrane, was significantly greater than in the augmented space at 2 and 4 weeks. We conclude that newly formed bone in the augmented space after grafting with blood clot is unstable during the early stage of bony regeneration.

Expression of tumor necrosis factor alpha, TNF-related apoptosis-inducing ligand, and their associated molecules in ameloblastomas.

BACKGROUND: To clarify the roles of the apoptosis signaling pathway mediated by death receptors in oncogenesis and cytodifferentiation of odontogenic tumors, expression of tumor necrosis factor alpha (TNFalpha), TNF-related apoptosis-inducing ligand (TRAIL), and their associated molecules was analyzed in ameloblastomas as well as in tooth germs. METHODS: Tissue specimens of 10 tooth germs, 40 benign ameloblastomas, and five malignant ameloblastomas were examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry to determine the expression of TNFalpha, TNF receptor I (TNFRI), TRAIL, TRAIL receptor 1 (TRAIL-R1), TRAIL-R2, caspase-8, and nuclear factor-kappaB (NF-kappaB). RESULTS: Expression of TNFalpha, TNFRI, TRAIL, TRAIL-R1, TRAIL-R2, and NF-kappaB mRNA was detected in most samples of normal and neoplastic odontogenic tissues. Expression of caspase-8 mRNA was identified in six of 33 ameloblastomas, but not in 10 tooth germs or one malignant ameloblastoma. Immunohistochemical reactivity for TNFalpha, TRAIL, their receptors, and NF-kappaB was detected in both normal and neoplastic odontogenic tissues. Epithelial expression of TNFalpha was focal in about 50% of tooth germs and ameloblastomas, and TNFalpha expression in neoplastic cells was significantly higher in follicular ameloblastomas than in plexiform ameloblastomas. TRAIL reactivity was evident in epithelial cells neighboring the basement membrane. Receptors for TNFalpha and TRAIL were diffusely expressed in both normal and neoplastic odontogenic epithelium. Expression of caspase-8 was found in some neoplastic cells in three of 37 ameloblastomas, but not in 10 tooth germs or five malignant ameloblastomas. Nuclear NF-kappaB expression was much lower than cytoplasmic expression in both normal and neoplastic odontogenic epithelium. CONCLUSION: Expression of TNFalpha, TRAIL, and their receptors in tooth germs and ameloblastomas suggests that these death factors might be involved in cytodifferentiation of odontogenic epithelium and tissue structuring of ameloblastomas. Expression of caspase-8 and NF-kappaB suggests that signaling of TNFalpha and TRAIL minimally affects the biological properties of odontogenic epithelial components.

Expression of p63 and p73 in ameloblastomas.

BACKGROUND: To clarify the role of p53 homologs in oncogenesis and cytodifferentiation of odontogenic tumors, expression of p63 and p73 was analyzed in ameloblastomas as well as tooth germs. METHODS: Tissue specimens of nine tooth germs and 48 benign and five malignant ameloblastomas were examined by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) for the expression of p63 and p73. RESULTS: Immunoreactivity for p63 and p73 was evident in epithelial cells neighboring the basement membrane in developing and neoplastic odontogenic tissues. p63 expression in desmoplastic ameloblastomas was significantly higher than in acanthomatous and granular cell ameloblastomas, and ameloblastic carcinomas showed higher p63 expression than metastasizing ameloblastomas. p73 expression was significantly higher in plexiform ameloblastomas than in follicular ameloblastomas, and basal cell ameloblastomas showed higher p73 expression than granular cell ameloblastomas. mRNA transcripts for Delta Np63 and TAp73 were detected in all developing and neoplastic odontogenic tissues. TAp63 mRNA was expressed in five of eight tooth germs, 16 of 34 ameloblastomas, and one of one malignant ameloblastoma, whereas Delta Np73 mRNA was recognized in one of eight tooth germs, nine of 34 ameloblastomas, and one of one malignant ameloblastoma. CONCLUSION: The expression of p63 and p73 suggests that these p53 homologs play a role in differentiation and proliferation of odontogenic epithelial cells. Variations of predominantly expressed isoforms suggest that p63 and p73 might differentially function in odontogenic tissues.

Blood-filled spaces with and without deproteinized bone grafts in guided bone regeneration. A histomorphometric study of the rabbit skull using non-resorbable membrane.

This experimental study evaluated the effects of deproteinized bone grafts on guided bone regeneration (GBR). A groove was made in the bone marrow of the external cortical plate of the skull. A dome of non-resorbable membrane was placed on the groove and secured with titanium pins. The secluded graft space was filled with autogenous blood clots (control group) and deproteinized bone particles (experimental group). The rabbits were sacrificed 2, 4, 8 and 12 weeks after the operation. Decalcified and paraffin-embedded, transverse 3-mum-thick sections were made and stained with hematoxylin and eosin. The proportions of newly formed bone and newly formed bone-graft particle contact surfaces were histomorphometrically measured in the basal, central, and peripheral areas from the cortical plate to the top of the dome. In the control group, the basal area showed a significant increase at 4 weeks (P<0.01) and a significant decrease at 8 weeks (P<0.01). The central and peripheral areas showed gradual increases in the proportion of newly formed bone. The experimental group showed significant increase at 4 weeks in the basal area and at 8 weeks in central and peripheral area (P<0.01). There were significant differences between both groups in basal and central area (P<0.01). The proportion of newly formed bone-graft particle contact length showed significant increases at 4 weeks (P<0.01) and no significant decreases at 8 and 12 weeks in three areas. The present study showed that deproteinized bone grafts maintain newly formed bone in extensive areas for a prolonged period during GBR.

Weight distributions on soles of feet in the primary and early permanent dentition with normal occlusion.

This study investigated the differences of weight distribution on the sole of the feet in the primary and the early permanent dentition by the modifying Morton staticometer. The distribution of body weight in the outer forward part on soles of feet in the permanent dentition group was significantly greater than that in the primary dentition group. The distribution of body weight in the heel on soles of feet in the permanent dentition group was significantly smaller than that in the primary dentition group. These results indicated that the weight was shifted from the heels to the forefeet from primary to permanent dentition.

Long-term outcome of augmentation of the maxillary sinus using deproteinised bone particles experimental study in rabbits.

We studied the long-term outcome of deproteinised bone particles for augmentation of the maxillary sinus in rabbits. Histologically, 64 weeks after implantation, most of the newly formed bone in the augmented spaces had been absorbed. Histomorphometric analysis showed a significant reduction in the area of bone and a significant increase in the area of bone marrow. There was no substantial change in the area of deproteinised bone particles. We conclude that deproteinised bone particles do not absorb with time and that the newly formed bone in the augmented space after implantation is not stable in the long-term.

Apoptosis-related factors in the epithelial components of dental follicles and dentigerous cysts associated with impacted third molars of the mandible.

OBJECTIVE: Radiolucencies adjacent to the crowns of impacted third molars can represent follicular remnants or cysts. To clarify the possible role of apoptosis-related factors in pericoronal odontogenic tissues, expression of Fas, bcl-2, and single-stranded DNA (ssDNA) was examined in epithelial components of dental follicles (DFs) and dentigerous cysts (DCs) associated with impacted third molars of the mandible. The results were compared with immunoreactivity for Ki-67, a marker of cell proliferation. STUDY DESIGN: Specimens of 80 DFs and 27 DCs were examined immunohistochemically using antibodies against Fas, bcl-2, ssDNA, and Ki-67. RESULTS: Expression of Fas and ssDNA was detected in superficial epithelial cells of DFs and DCs. Expression of bcl-2 and Ki-67 was found in epithelial cells neighboring the basement membrane. The positive ratio of bcl-2 in DFs was significantly lower than that in DCs. ssDNA-positive cells were slightly more numerous in DFs, while Ki-67-positive cells were slightly more numerous in DCs. In DFs, epithelial tissues with proliferative rete processes showed significantly higher Ki-67 labeling than did those without proliferative rete processes. DFs with marked inflammatory changes showed slightly higher rates of ssDNA and Ki-67 positivity than did DFs without marked inflammation. CONCLUSIONS: Apoptosis-related factors and proliferative marker differ between DFs and DCs. Apoptosis and cell proliferation may play a role in the pathogenesis of DCs. In DFs, expression of apoptosis-related factors and proliferative marker is most likely modulated by the morphologic characteristics of epithelial components as well as by inflammatory changes.

An evaluation of the curve of Spee in the maxilla and mandible of human permanent healthy dentitions.

STATEMENT OF PROBLEM: The characteristics of the curve of Spee in the mandibular arch have been extensively investigated. However, few studies have examined the characteristics of the curve of Spee in the maxillary arch. PURPOSE: The purpose of this study was to examine the differences in the curve of Spee between the maxillary and mandibular arches. The effects of gender on the curve of Spee were also investigated. Material and methods Fifty Japanese adults (25 men and 25 women) with permanent healthy dentitions participated. Standardized digital pictures of the right side of maxillary and mandibular dental casts were made with a digital camera. The cusp tips of the molars, premolars, and canines of the maxilla and mandible were identified. The radius and the depth of the curve of Spee were measured on the dental casts by means of computer software (Occlcircle). The Mann-Whitney test and the Wilcoxon signed rank test were used to test the statistical significance (alpha=.05). RESULTS: The curve of Spee showed a mean radius of approximately 106.4 mm in the maxillary arch and 83.4 mm in the mandibular arch. Radii of the curves of Spee in the maxillary arch were significantly larger than those in the mandibular arch (P <.0001) and had a depth of approximately 1.6 mm in the maxillary arch and 1.9 mm in the mandibular arch. The depth of the curve of Spee in the mandibular arch was significantly deeper than that in the maxillary arch (P =.0326). CONCLUSIONS: The curve of Spee was not influenced by the gender of the subjects investigated. The shape of the curve of Spee in the maxillary arch was significantly flatter than that in the mandibular arch.

K-Ras gene status and expression of Ras/mitogen-activated protein kinase (MAPK) signaling molecules in ameloblastomas.

BACKGROUND: To clarify the roles of rat sarcoma (Ras)/mitogen-activated protein kinase (MAPK) signaling pathway in oncogenesis and cytodifferentiation of odontogenic tumors, K-Ras gene status and expression of Ras, Raf1, MAPK/extracellular signal-regulated kinase (ERK) kinase (MEK)1, and ERK1/2 proteins were analyzed in ameloblastomas as well as in tooth germs. METHODS: Paraffin sections of 10 tooth germs and 46 benign and 6 malignant ameloblastomas were examined immunohistochemically for the expression of K-Ras, Raf1, MEK1, and ERK1/2. Frozen tissue samples of 22 benign ameloblastomas and 1 malignant (metastasizing) ameloblastoma were analyzed by direct DNA sequencing to detect K-Ras gene alteration. RESULTS: Immunohistochemical reactivity for K-Ras, Raf1, MEK1, and ERK1/2 was detected in both normal and neoplastic odontogenic epithelium, and these molecules were reactive chiefly with odontogenic epithelial cells neighboring the basement membrane. Plexiform ameloblastomas showed slightly stronger expression of these Ras/MAPK signaling molecules than follicular ameloblastomas. Keratinizing cells and granular cells showed decreased reactivity for the signaling molecules. Basal cell ameloblastomas showed slightly stronger reactivity for the signaling molecules than did the other subtypes. K-Ras immunoreactivity in malignant ameloblastomas was lower than that in dental lamina of tooth germs. Direct DNA sequencing showed a GGT to GCT point mutation at codon 12 of K-Ras gene in one ameloblastoma. CONCLUSION: Expression of K-Ras, Raf1, MEK1, and ERK1/2 in tooth germs and ameloblastomas suggests that Ras/MAPK signaling pathway functions to regulate cell proliferation and differentiation in both normal and neoplastic odontogenic epithelium. K-Ras gene status implied that K-Ras mutations might play a minor role in oncogenesis of odontogenic epithelium.

Expression of Sonic hedgehog (SHH) signaling molecules in ameloblastomas.

BACKGROUND: To clarify the roles of Sonic hedgehog (SHH) signal transduction in oncogenesis and cytodifferentiation of odontogenic tumors, expression of SHH, Patched (PTC), Smoothened (SMO), and GLI1 was analyzed in ameloblastomas as well as in tooth germs. METHODS: Tissue specimens of 9 tooth germs, 36 benign ameloblastomas, and 1 malignant ameloblastoma were examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry for the expression of SHH, PTC, SMO, and GLI1. RESULTS: Expression of SHH, PTC, SMO, and GLI1 mRNA was detected in all tooth germ and ameloblastoma samples. Immunohistochemical reactivity for SHH, PTC, SMO, and GLI1 was detected in both normal and neoplastic odontogenic tissues. Expression of SHH, PTC, and GLI1 was more evident in epithelial cells than in mesenchymal cells, whereas SMO reactivity was marked in both epithelial and mesenchymal components in tooth germs and ameloblastomas. In ameloblastomas, these SHH signaling molecules were expressed more intensely in peripheral columnar or cuboidal cells than in central polyhedral cells; keratinizing cells and granular cells showed no or little reactivity. CONCLUSION: Expression of SHH, PTC, SMO, and GLI1 in tooth germs and ameloblastomas suggests that these SHH signaling molecules might play a role in epithelial-mesenchymal interactions and cell proliferation in tooth development as well as in growth of these epithelial odontogenic tumors.

Effects of cortical bone perforation on experimental guided bone regeneration.

This study was designed to evaluate the effects of cortical bone perforation histologically and histomorphometrically on guided bone regeneration (GBR) in rabbits. After elimination of the periosteum, cortical bone defects of two sizes were made in the external cortical plate of the frontal bone (Group A: 1 x 15 mm; Group B: 3 x 15 mm). A non-resorbable membrane filled with autogenous blood was placed in the experimental area and secured with titanium pins. After 1 and 2 weeks, vascularized connective tissue and new bone were generated in the space surrounding the defects in both the groups. The amount of vascularized connective tissue generated in Group B was greater than that in Group A at 1 week. Alkaline phosphatase (ALP) was expressed on the bone surrounding the perforation. The expression of ALP was more extensive in Group B than in Group A and was proportional to the breadth of perforation. At 2 weeks, the perforated region was almost covered with new bone in Group A. ALP was expressed at the periphery of newly formed bone. The expression of ALP was proportional to the breadth and height of perforation. At 6 weeks, semicircular outgrowth of bone towards the periphery of the perforated region was observed in both the groups. Newly formed bone volume and ALP expression in Group B were more extensive than those in Group A. At 12 weeks, the space was filled with bone and connective tissue in both the groups. There was no difference in ALP expression between Groups A and B. Histomorphometric analysis showed significant differences between both the groups (two-way ANOVA, P<0.01). We conclude that a larger perforation is associated with prompter bone formation in the secluded space during GBR.

A clinical long-term radiographic evaluation of graft height changes after maxillary sinus floor augmentation with a 2:1 autogenous bone/xenograft mixture and simultaneous placement of dental implants.

The aim of the present study was to assess long-term changes in sinus-graft height after maxillary sinus floor augmentation and simultaneous placement of implants. A total of 191 patients who underwent maxillary sinus floor augmentation were radiographically followed for up to about 10 years. A 2 : 1 mixture of autogenous bone and bovine xenograft (Bio-Oss) was used as the graft material. Sinus-graft height was measured using 294 panoramic images immediately after augmentation and up to 108 months subsequently. Changes in sinus-graft height were calculated with respect to implant length and original sinus height. Patients were divided into three groups based on the height of the grafted sinus floor relative to the implant apex: Group I, in which the grafted sinus floor was above the implant apex; Group II, in which the implant apex was level with the grafted sinus floor; and Group III, in which the grafted sinus floor was below the implant apex. After augmentation, the grafted sinus floor was consistently located above the implant apex. After 2-3 years, the grafted sinus floor was level with or slightly below the implant apex. This relationship was maintained over the long term. Sinus-graft height decreased significantly and approached original sinus height. The proportion of patients classified as belonging to Group III reached a maximum from year 3 onwards. The clinical survival rate of implants was 94.2%. All implant losses occurred within 3 years after augmentation. We conclude that progressive sinus pneumatization occurs after augmentation with a 2 : 1 autogenous bone/xenograft mixture, and long-term stability of sinus-graft height represents an important factor for implant success.

p53 gene status and expression of p53, MDM2, and p14 proteins in ameloblastomas.

BACKGROUND: To clarify the roles of the p53-MDM2-p14(ARF) cell cycle regulation system in oncogenesis and cytodifferentiation of odontogenic tumors, p53 gene status and expression of p53, MDM2, and p14(ARF) proteins was analyzed in ameloblastomas as well as tooth germs. METHODS: Paraffin sections of 16 tooth germs and 46 benign and 5 malignant ameloblastomas were examined immunohistochemically for the expression of p53, MDM2, and p14(ARF) proteins. Frozen tissue samples of 10 benign ameloblastomas and 1 malignant (metastasizing) ameloblastoma were analyzed by direct DNA sequencing to detect p53 gene alteration. RESULTS: Immunohistochemical reactivity for p53 was detected in 2 of 13 tooth germs, 13 of 29 ameloblastomas, and 5 of 5 malignant ameloblastomas, and the expression ratio of p53 in tooth germs was significantly lower than those in benign and malignant ameloblastomas. Direct DNA sequencing showed no alteration of p53 gene exons 5-8 in any sample of 10 benign ameloblastomas and 1 metastasizing ameloblastoma. Expression of MDM2 and p14(ARF) was detected in all samples of normal and neoplastic odontogenic epithelium, and the expression ratios in tooth germs tended to be lower than those in benign and malignant ameloblastomas. In ameloblastomas, expression of p53, MDM2, and p14(ARF) was significantly higher in plexiform cases than in follicular cases. Markedly decreased reactivity for p53, MDM2, and p14(ARF) was detected in keratinizing and granular cells in ameloblastoma subtypes. Basal cell ameloblastoma showed slightly higher reactivity for p53, MDM2, and p14(ARF) as compared with other subtypes. CONCLUSION: Elevated expression of p53, MDM2, and p14(ARF) in benign and malignant ameloblastomas suggests that alteration of the p53-MDM2-p14(ARF) cascade is involved in oncogenesis and/of malignant transformation of odontogenic epithelium. p53 gene status implied that p53 mutation might play a minor role in neoplastic changes of odontogenic epithelium. Immunoreactivity for p53, MDM2, and p14(ARF) in ameloblastoma variants suggests that these factors might be associated with tissue structuring and cytodifferentiation of ameloblastomas.

Grafting of deproteinized bone particles inhibits bone resorption after maxillary sinus floor elevation.

OBJECTIVES: To evaluate the value of deproteinized bone particles on bone resorption in the augmented space after maxillary sinus floor elevation in rabbits. MATERIAL AND METHODS: A total of 20 rabbits underwent bilateral grafting, using blood clots (control group) and deproteinized bone particles (experimental group), and followed with histologic and histomorphometric analysis. RESULTS: Two weeks after grafting, the augmented space was almost completely obliterated by both newly formed bone and fibrous connective tissue in the control group. Some osteoclasts were found on the surface of newly formed bone, especially near the elevated sinus membrane. In the experimental group, newly formed bone was found along the elevated sinus membrane, the cortical wall of the augmented space, and the surface of deproteinized bone particles near the cortical wall. Some osteoclasts were found along the deproteinized bone particles and a few adhered to the surface of the newly formed bone. Eight to 10 weeks after implantation in the control group, most of the newly formed bone had been resorbed. In the experimental group, newly formed bone was found in most parts of the convex augmented space. Histomorphometrical analysis showed that the augmented height was significantly higher in the experimental group than in the control group at all evaluation times. Bone area was significantly higher in the experimental group than in the control group at 6, 8, and 10 weeks after implantation. The area of grafted deproteinized bone particles did not change significantly from 2 to 10 weeks. CONCLUSION: Slowly resorbed deproteinized bone particles contribute to stable augmentation of the maxillary sinus floor by inhibiting bone resorption.

Benign cementoblastoma involving multiple maxillary teeth: report of a case with a review of the literature.

A rare case of benign cementoblastoma involving multiple deciduous and permanent teeth is presented with a review of the literature. A 12-year-old boy was admitted for a swelling in the right maxillary premolar-molar region. A radiologic examination revealed a well-defined, round, radiopaque mass extending from the right maxillary first premolar to the second permanent molar. The tumor was removed with all associated teeth. A histologic examination of the surgical specimen revealed a well-circumscribed tumor composed of cementum-like tissue surrounded by a fibrous capsule. The tumor was attached to the roots of the second deciduous molar, first premolar, and the first and second permanent molars and embedded in the crown and root of the right maxillary second premolar, suggesting that the lesion had arisen from the second deciduous molar. There has been no recurrence of the lesion more than 18 months after the surgical procedure.