Factors Affecting the Occurrence of Complications in the Early Stages After Dental Implant Placement: A Retrospective Cohort Study.

OBJECTIVE: To evaluate the background factors related to the occurrence of complications in the early stages after dental implant placement. MATERIALS AND METHODS: A total of 289 outpatients who received dental implants were retrospectively evaluated for the presence or absence of complications. Background factors, including age, sex, implant width, implant length, implant site, number of implants placed, Periotest values at the time of implant placement, presence/absence of systemic disease (particularly diabetes), and the use of anticoagulation therapy, were compared between patients with and without complications. Logistic regression analysis was performed to identify significant risk factors for the occurrence of complications after dental implant placement. RESULTS: Complications in the early stages after dental implant placement occurred in 25 (8.65%) patients. The patients with complications were older than those without complications (P = 0.003). In addition, the incidence of complications was significantly higher in patients with systemic diseases (P = 0.004) and in those receiving anticoagulation therapy (P = 0.005). Logistic regression analysis revealed that age was a significant risk factor (P = 0.025) for early-stage complications, whereas the number of implants, presence of diabetes, and the use of anticoagulation therapy were not significant risk factors. CONCLUSIONS: Our results show that age is a significant factor influencing the occurrence of complications in the early stages after dental implant placement. Therefore, clinicians should consider this factor when developing their treatment strategies.

A toothbrush impalement injury of the floor of mouth in autism child.

Penetrating injuries in the oral cavity are common in children. However, penetrating injuries with retained foreign bodies are rare. We report a case of a toothbrush impalement injury of the floor of the mouth in a child with autism. A 5-year-old boy with autism presented with an accidentally impaled toothbrush in the oral cavity. He was taken to the operation room and examined under general anesthesia. The handle of the toothbrush was cut off using rib scissors for mask ventilation, and intra-oral intubation was performed. The toothbrush was located approximately 2.5 cm into the floor of the mouth. The toothbrush was removed uneventfully. Intravenous antibiotic therapy was instituted during hospitalization, and discharge from the hospital occurred 4 days after the operation.

Long-term exposure to superantigen induces p27Kip1 and Bcl-2 expression in effector memory CD4+ T cells.

The long-term exposure of mice to superantigen SEA using a mini-osmotic pump (SEA pump) induced a long-lasting expansion of Vbeta3+ CD4+ T cells with T helper (Th) 2 cell-type properties. Removal of the SEA pump 10 days after pump implantation did not significantly alter the level of Vbeta3+ CD4+ T cell expansion/maintenance. Furthermore, CFSE-labeled CD4+ T cells failed to divide when transferred to post-implantation day 15 mice. Thus, CD4+ T cells appeared to survive for at least 30 days in the absence of a sufficient amount of antigen to trigger cell division. STAT6 deficient mice, in which Th2 cell development is largely impaired, also exhibited a protracted cell expansion, similar to that observed in normal mice, suggesting that the Th2 cell property is dispensable for the maintenance of Vbeta3+ CD4+ T cell expansion. The expanded CD4+ T cells on post-implantation day 26 were arrested in the G0/G1 phase of the cell cycle and showed a lower level of cell division upon restimulation. The Cdk inhibitor p27(Kip1) was highly expressed, and Cdk2 was downregulated. Moreover, the CD4+ T cells were resistant to in vitro apoptosis induction in parallel with their level of Bcl-2 expression. Collectively, the Vbeta3+ CD4+ T cells appeared to develop into long-lived memory T cells with cell cycle arrest upon long-term exposure to SEA.

CD28 is required for induction and maintenance of immunological memory in toxin-reactive CD4+ T cells in vivo.

We previously reported that Vbeta3+ CD4+ T cells maintained a protracted expansion, with the phenotypes of memory Th2 cells, for 30 days in C57BL/6 (B6) mice implanted with SEA-containing mini-osmotic pumps. In the present study, we followed the fate of Vbeta3+ CD4+ T cells in CD28-/- mice. Vbeta3+ CD4+ T cells increased to a degree similar to that of B6 Vbeta3+ CD4+ T cells until day 10 after implantation, then declined rapidly reaching the control level by 28 days. Remaining Vbeta3+ CD4+ T cells at that time did not exhibit memory phenotypes nor Th2-deviated responses. The rapid drop in Vbeta3+ CD4+ T cells in CD28-/- mice was attributable to upregulated induction of apoptosis owing to marginal inductions of Bcl-2 and Bcl-xL. Collectively, these data indicate CD28 to play critical roles in the generation and maintenance of SEA-reactive CD4+ T cells in vivo.

Mandibular coronoid process in parathyroid hormone-related protein-deficient mice shows ectopic cartilage formation accompanied by abnormal bone modeling.

Parathyroid hormone-related protein (PTHrP) null mutant mice were analyzed to investigate an additional role for PTHrP in cell differentiation. We found ectopic cartilage formation in the mandibular coronoid process in newborn mice. While many previous studies involving PTHrP gene knockout mouse have shown that the cartilage in various regions becomes smaller, this is the first report showing an "increase" of cartilage volume. Investigations of mandibular growth using normal mice indicated that coronoid secondary cartilage never formed from E 15 to d 4, but small amount of cartilage temporally formed at d 7, and this also applies to PTHrP-wild type mice. Therefore, PTHrP deficiency consequently advanced the secondary cartilage formation, which is a novel role of PTHrP in chondrocyte differentiation. In situ hybridization of matrix proteins showed that this coronoid cartilage had characteristics of the lower hypertrophic cell zone usually present at the site of endochondral bone formation and/or "chondroid bone" occasionally found in distraction osteogenesis. In addition, the coronoid process in the PTHrP-deficient mouse also showed abnormal expansion of bone marrow and an increase in the number of multinucleated osteoclasts, an indication of abnormal bone modeling. These results indicate that PTHrP is involved in bone modeling as well as in chondrocyte differentiation. In situ hybridization of matrix protein mRNAs in the abnormal mandibular condylar cartilage revealed that this cartilage was proportionally smaller, supporting previous immunohistochemical results.

Localization and inhibitory effect of basic fibroblast growth factor on chondrogenesis in cultured mouse mandibular condyle.

The condylar cartilage, an important growth site in the mandible, shows characteristic modes of growth and differentiation, unlike the limb bud cartilage. To elucidate the mechanism of chondrogenesis at the condylar cartilage, we analyzed the effects of basic fibroblast growth factor (bFGF) on the growth and development of mouse mandibular condyle using serum-free organ culture and on the expression of genes related to the chondrogenesis. Further, we investigated the localization of bFGF in cultured condyle by immunohistochemistry. The present immunohistochemical observations showed that bFGF is localized in the extracellular matrix of the mesenchymal condylar anlage, the perichondrium and the proliferative cell zone, and that immunostaining was diminished in the metachromatically stained area. In the condyle culture with added recombinant human bFGF (rhbFGF) for 5 days, the area occupied by hypertrophic chondrocytes in the mandibular condylar cartilage was reduced. A reverse transcription-polymerase chain reaction (RT-PCR) assay also showed that the mRNA levels of aggrecan and type X collagen were reduced compared with nontreated tissues. Treatment with rhbFGF for 2 days decreased cell proliferation in the perichondrium, and bFGF downregulated the Indian hedgehog (Ihh), parathyroid hormone-related protein (PTHrP), bone morphogenetic protein 4 (BMP4), and core-binding factor alpha1 (Cbfa1) expression in the RT-PCR assay. These findings suggest that bFGF has the ability for inhibitory regulation of condylar growth, via the inhibition of proliferation and differentiation of chondrocytes, and that this inhibitory regulation is related to the downregulation of growth factors and transcription factors.

Immunohistochemical localization of matrix metalloproteinase 13 (MMP-13) in mouse mandibular condylar cartilage.

MMP-13 appears to be one of the most important MMPs in cartilage remodeling and mineralization, because it exhibits a substrate preference for the cartilage-specific type II collagen. The condylar process is constructed by rapid accumulation of hypertrophic chondrocytes during development, but its mechanism is still unclear. To investigate the role of MMP-13 in developing condylar cartilage, we immunohistochemically examined the localization of MMP-13 in the endochondral ossification of the mandibular condyle and tibiae of newborn mice. In the tibiae, the MMP-13 expression was detected only in the deepest layer of the terminal hypertrophic chondrocytes through every examined stage (day 1 to day 10 after birth). On the other hand, in the condylar cartilage at days 1 and 5, MMP-13 was expressed throughout the proliferating and the hypertrophic chondrocytes, and at day 10, MMP-13 was mainly localized in the deepest edge of the hypertrophic layer. A zymographical study showed that the activity of MMP-13 in the condyle was observed at day 1, earlier than in the tibia, and increased until day 7. The time-dependent and cell-specific expression of MMP-13 and its enzymatic property suggest that in the mandibular condylar cartilage, MMP-13 plays a role in making the space for cell enlargement by degradation of the cartilage matrix and in onset of mineralization during the early stage of development.

In situ hybridization and immunohistochemistry of bone sialoprotein and secreted phosphoprotein 1 (osteopontin) in the developing mouse mandibular condylar cartilage compared with limb bud cartilage.

Mandibular condylar cartilage is often classified as a secondary cartilage, differing from the primary cartilaginous skeleton in its rapid progress from progenitor cells to hypertrophic chondrocytes. In this study we used in situ hybridization and immunohistochemistry to investigate whether the formation of primary (tibial) and secondary (condylar) cartilage also differs with respect to the expression of two major non-collagenous glycoproteins of bone matrix, bone sialoprotein (BSP) and secreted phosphoprotein 1 (Spp1, osteopontin). The mRNAs for both molecules were never expressed until hypertrophic chondrocytes appeared. In the tibial cartilage, hypertrophic chondrocytes first appeared at E14 and the expression of BSP and Spp1 mRNAs was detected in the lower hypertrophic cell zone, but the expression of BSP mRNA was very weak. In the condylar cartilage, hypertrophic chondrocytes appeared at E15 as soon as cartilage tissue appeared. The mRNAs for both molecules were expressed in the newly formed condylar cartilage, although the proteins were not detected by immunostaining; BSP mRNA in the condylar cartilage was more extensively expressed than that in the tibial cartilage at the corresponding stage (first appearance of hypertrophic cell zone). Endochondral bone formation started at E15 in the tibial cartilage and at E16 in the condylar cartilage. At this stage (first appearance of endochondral bone formation), BSP mRNA was also more extensively expressed in the condylar cartilage than in the tibial cartilage. The hypertrophic cell zone in the condylar cartilage rapidly extended during E15-16. These results indicate that the formation process of the mandibular condylar cartilage differs from that of limb bud cartilage with respect to the extensive expression of BSP mRNA and the rapid extension of the hypertrophic cell zone at early stages of cartilage formation. Furthermore, these results support the hypothesis that, in vivo, BSP promotes the initiation of mineralization.

Continuous exposure of mice to superantigenic toxins induces a high-level protracted expansion and an immunological memory in the toxin-reactive CD4+ T cells.

We analyzed the responses of several T cell fractions reactive with superantigenic toxins (SAGTs), staphylococcal enterotoxin A (SEA), or Yersinia pseudotuberculosis-derived mitogen (YPM) in mice implanted with mini-osmotic pumps filled with SEA or YPM. In mice implanted with the SEA pump, SEA-reactive Vbeta3(+)CD4(+) T cells exhibited a high-level protracted expansion for 30 days, and SEA-reactive Vbeta11(+)CD4(+) T cells exhibited a low-level protracted expansion. SEA-reactive CD8(+) counterparts exhibited only a transient expansion. A similar difference in T cell expansion was also observed in YPM-reactive T cell fractions in mice implanted with the YPM pump. Vbeta3(+)CD4(+) and Vbeta11(+)CD4(+) T cells from mice implanted with the SEA pump exhibited cell divisions upon in vitro restimulation with SEA and expressed surface phenotypes as memory T cells. CD4(+) T cells from mice implanted with the SEA pump exhibited high IL-4 production upon in vitro restimulation with SEA, which was due to the enhanced capacity of the SEA-reactive CD4(+) T cells to produce IL-4. The findings in the present study indicate that, in mice implanted with a specific SAGT, the level of expansion of the SAGT-reactive CD4(+) T cell fractions varies widely depending on the TCR Vbeta elements expressed and that the reactive CD4(+) T cells acquire a capacity to raise a memory response. CD8(+) T cells are low responders to SAGTs.

[Combination chemotherapy with nedaplatin (CDGP) and 5-FU for oral cancer].

Chemotherapy using CDGP plus 5-FU was evaluated in patients with oral cancer. The subjects were patients with squamous cell carcinoma of the oral cavity who had not received any therapy, comprising 7 patients with carcinoma of the tongue, 2 with buccal carcinoma, 2 with maxillary gingival carcinoma, and 1 with carcinoma of the oral floor. There were 4 patients in Stage II, 3 patients in Stage III and 5 patients in Stage IV. Patients with a PS < or = 1, WBC > or = 4,000/mm3, Hb > or = 10 g/dl, platelet count > or = 10 x 10/mm3, and normal liver, kidney, and heart function at baseline were selected for this study. In all patients, 5-FU was administered at a dose of 600 mg/m2/day for 5 days (day 1 to day 5) by continuous infusion, for a total dose of 3,000 mg/m2. CDGP was administered on day 1 at a dose of 80 mg/m2 in 8 patients and at 100 mg/m2 in 4 patients. This treatment was one course of therapy, and patients received 1 or 2 courses. Of 12 patients who were evaluable, there were 9 partial responses and 3 no changes, for a major response rate of 75%. Toxicities experienced by patients were mild (grade 2 or lower) gastrointestinal disorders (including nausea/vomiting) and renal impairment, while grade 3 leukopenia and thrombocytopenia developed in 1 patient each and grade 4 thrombocytopenia occurred in another patient. Thus, patients receiving CDGP + 5-FU therapy should be closely monitored for hematologic toxicity. Since CDGP + 5-FU therapy achieved a good response rate (75%) in the treatment of squamous cell carcinoma of the oral cavity, we plan to use this therapy in the future and assess its benefit in a larger number of patients.

Three cases of anterior maxillary osteotomy under orotracheal intubation.

Anterior maxillary osteotomy is frequently applied to skeletal Class II cases with maxillary protrusion. In addition to the anteroposterior problem, these cases are often accompanied with a long midfacial appearance and display of incisors and gingiva during smiling. In the application of anterior maxillary osteotomy to such patients, it is necessary to move the anterior maxillary segments upward as well as backward. Since the upward movement occasionally interferes with the intranasal endotracheal tube, orotracheal intubation is recommended for the operation. Recently, the use of a resin replica of the mandibular dental arch was introduced to place the anterior maxillary segment correctly in the planned position and to obtain the correct occlusion. This article reports on 3 maxillary protrusive skeletal Class II patients with deep overbites and vertical esthetic problems treated by this method. The treatment results show that all 3 patients exhibited large upward and backward movements of the anterior maxillary segments and desirable facial profiles, with a reduction of the deep overbites after the treatment. This case report demonstrates that the anterior maxillary osteotomy under orotracheal intubation with the use of a resin replica is a useful method to treat maxillary protrusive skeletal Class II patients with a large alveolar height.