Clinical retrospective study of dental implant removal: do patients who require implant removal desire implant prosthesis again?

BACKGROUND: This study investigated the causes of dental implant removal due to complications, and examined whether patients who had dental implant removal desired re-implant prosthesis treatments. MATERIAL AND METHODS: A retrospective case-control study was conducted on patients who had their dental implants removed. We investigated whether the removed dental implant was replaced with other implant prostheses. Age, sex, diabetes, smoking, implant site distribution, reason for implant removal, and blade and root-form implants were categorized as predictive variables. The outcome variable was desire for re-implantation or use of other prosthetic methods after implant removal. A logistic regression model was created to identify patient factors that could predict the re-implantation of dental prostheses after implant removal. RESULTS: A total of 215 dental implants were removed from 143 patients. The most common reason for implant removal was peri-implantitis that was identified in 165 implants. After implant removal, re-implantation was performed in 98 implants (45.6%). Bivariate analyses showed that age, diabetes, implant type, and reason for implant removal were associated with the desire for re-implanted prostheses. The multiple regression model revealed that age, implant type, and reason for implant removal were associated with an increased desire for re-implant prostheses after implant removal. CONCLUSIONS: Re-implantation of prostheses after the removal of dental implants was desired by patients who were younger, had implants placed in the root form, and had implants removed due to prosthetic-related complications.

SETBP1 mutations drive leukemic transformation in ASXL1-mutated MDS.

Mutations in ASXL1 are frequent in patients with myelodysplastic syndrome (MDS) and are associated with adverse survival, yet the molecular pathogenesis of ASXL1 mutations (ASXL1-MT) is not fully understood. Recently, it has been found that deletion of Asxl1 or expression of C-terminal-truncating ASXL1-MTs inhibit myeloid differentiation and induce MDS-like disease in mice. Here, we find that SET-binding protein 1 (SETBP1) mutations (SETBP1-MT) are enriched among ASXL1-mutated MDS patients and associated with increased incidence of leukemic transformation, as well as shorter survival, suggesting that SETBP1-MT play a critical role in leukemic transformation of MDS. We identify that SETBP1-MT inhibit ubiquitination and subsequent degradation of SETBP1, resulting in increased expression. Expression of SETBP1-MT, in turn, inhibited protein phosphatase 2A activity, leading to Akt activation and enhanced expression of posterior Hoxa genes in ASXL1-mutant cells. Biologically, SETBP1-MT augmented ASXL1-MT-induced differentiation block, inhibited apoptosis and enhanced myeloid colony output. SETBP1-MT collaborated with ASXL1-MT in inducing acute myeloid leukemia in vivo. The combination of ASXL1-MT and SETBP1-MT activated a stem cell signature and repressed the tumor growth factor-ß signaling pathway, in contrast to the ASXL1-MT-induced MDS model. These data reveal that SETBP1-MT are critical drivers of ASXL1-mutated MDS and identify several deregulated pathways as potential therapeutic targets in high-risk MDS.

Distinct gene expression in the stomach following stress and alcohol exposure.

Two paradigms of acute stress in the rat were used to produce changes in the stomach. The first involved restraint stress combined with water immersion and the second utilized acute intragastric exposure to absolute ethanol. The mRNA expression of immediate early genes (IEG) such as c-fos, c-jun and NGFI-A, cyclooxygenase (COX)-2 and heat shock proteins (HSP) 70 in the stomach were studied using in situ hybridization histochemistry. Upregulation of IEG and HSP70 mRNAs were observed in the smooth muscle cells of muscularis mucosae, muscularis externa and blood vessels in response to water immersion-restraint stress or intragastric application of absolute ethanol. In the restraint stress model, IEG (c-fos and NGFI-A) mRNAs were induced in the pit and isthmus of the mucosa, while in the ethanol exposure model, IEG (c-fos, c-jun and NGFI-A) and HSP70 mRNAs were upregulated in the damaged epithelium, especially surrounding the deep erosions. COX-2 mRNA was detected in surface mucous cells under desquamation. These distinct gene expressions in the mucosa indicate that the two stress paradigms produce different cellular responses. These data provide new insights into cellular mechanisms that occur during the pathogenesis of acute gastric mucosal lesions.

17beta-estradiol stimulates expression of osteoprotegerin by a mouse stromal cell line, ST-2, via estrogen receptor-alpha.

Osteoprotegerin (OPG) is a recently identified member of the tumor necrosis factor (TNF) receptor superfamily that regulates bone mass through an inhibitory action on osteoclast differentiation and function. To determine its potential roles of OPG in pathological changes in bone metabolism caused by estrogen deficiency, we investigated effects of estrogen on OPG expression by a mouse stromal cell line, ST-2, in vitro. Treatment of ST-2 cells with 17beta-E(2) resulted in up-regulation of OPG expression at both the messenger RNA and protein levels. The effect was time and dose dependent and steroid specific. The stimulatory action of 17beta-E(2) on OPG expression appeared to be mediated by the estrogen receptor-alpha (ERalpha) subtype because stable overexpression of ERalpha, but not of ERbeta, enhanced the OPG induction by 17beta-E(2). Moreover, estrogen withdrawal after 5-day pretreatment, mimicking the event occurring in vivo at menopause, dramatically diminished the expression of OPG. These findings suggest that down-regulation of OPG after estrogen withdrawal contributes to the enhanced osteoclastic bone resorption and bone loss after menopause by enhancing RANK ligand-RANK system that lies downstream of a large number of bone-resorbing cytokines.

Expression of immediate early genes, HSP70, and COX-2 mRNAs in rat stomach following ethanol ingestion.

The aim of this study was to show the temporal and spatial molecular responses in the rat stomach that follow absolute ethanol-induced acute mucosal injury. Intense signals for immediate early genes (IEG)/transcriptional factors such as c-fos, c-jun, and nerve growth factor-induced gene-A (NGFI-A) mRNAs were observed in the superficial mucosa and in the blood vessels from 15 min to 6 hr after administration, peaking at 15-30 min. Signals for heat shock protein (HSP) 70 mRNA were also detected in the superficial mucosa, in the fibroblasts around gastric erosions, and in the blood vessels from 15 min to 6 hr (peak at 1-2 hr). The signals for cyclooxygenase-2 (COX-2) mRNA were up-regulated in the surface mucous cells that surround the erosions from 30 min to 6 hr (peak at 60-90 min). These findings suggest that IEG, HSP70, and COX-2 are involved in gastric mucosal restitution in different ways.

Prostacyclin analog prevents stress-induced expression of immediate early genes and gastric mucosal lesions in the rat stomach.

Water immersion-restraint induced the expression of immediate early genes (IEGs) in the epithelial cells and smooth muscle cells of gastric wall of rats, in addition to its well-known effects of mucosal erosion. Pretreatment with a prostacyclin analog (beraprost), a proton pump inhibitor (lansoprazole) or a histamine H2 receptor antagonist (famotidine) prevented formation of gastric mucosal erosion, while only the prostacyclin analog inhibited expression of IEGs. The prostacyclin analog may prevent mucosal damages as well as molecular changes by ameliorating the mucosal microcirculation, and may have potential therapeutic applications.

Water immersion-restraint stress induces expression of immediate-early genes in gastrointestinal tract of rats.

The aims of this study were to determine 1) which cells are involved in stress-induced acute gastric mucosal lesion and 2) what kinds of molecular alterations are induced by stress, using immediate-early genes (IEG) as tools for detection of cellular activation. Male Wistar rats were exposed to acute water immersion-restraint stress. Protein and mRNA for IEG were detected by immunohistochemistry and in situ hybridization, respectively. This stress induced the expression of c-fos and nerve growth factor-induced gene (NGFI-A) mRNA in gastric epithelial cells, the smooth muscle layer of small blood vessels, and the stomach wall. Stress upregulated the mRNA levels of these IEG in the duodenal epithelial cells and induced de novo expression of IEG in the smooth muscle layer of small blood vessels and the duodenal wall. These findings indicate that these cells are activated in response to stress. Expression of these IEG and/or transcriptional factors may reflect an initiation of mechanisms for repairing the lesions induced by stress as well as an adaptation to the stress.

Intradermal 5-HT induces Fos expression in rat dorsal horn neurons not via 5-HT3 but via 5-HT2A receptors.

We investigated the effects of peripherally administered 5-HT on the secondary neurons in the spinal cord of rats using Fos-like immunoreactivity (FLI) as a marker of neuronal activation. The intradermal administration of 5-HT (30, 60 microg) induced a large number of FLI neurons in the ipsilateral dorsal horn. In animals given 5-HT2A receptor agonists (DOI: 0.28 to 2.8 micromol/kg, alpha-methyl 5-HT: 0.28 to 2.8 micromol/kg) intradermally, immunoreactive neurons were evoked in the same manner as those given 5-HT. Other agonists, including 5-HT3 receptor agonists (m-CPG: 16 to 32 micromol/kg, 2-methyl 5-HT: 0.0028 to 2.8 micromol/kg), did not induce FLI neurons at any dose examined. Furthermore, 5-HT2A receptor antagonist (ketanserin: 1 mg/kg, i.p.) suppressed the expression of FLI in the dorsal horn caused by peripheral 5-HT, but 5-HT3 receptor antagonist (tropisetron: 1 mg/kg, i.p.) did not. These findings suggest that the 5-HT-induced nociceptive response is mediated by 5-HT2A receptors in the periphery.

Cervical laminoplasty (Hattori's method). Procedure and follow-up results.

Posterior decompression plus posterior reconstruction (laminoplasty) is a useful surgical method for treatment of cervical compressive myelopathy. There are many laminoplasty procedures. This paper describes the Z-shaped laminoplasty developed by Hattori in 1971, and presents a clinical follow-up of the authors' experience with 130 patients. The procedure involves grinding the laminae down with an air drill and making a Z-shaped cut into the thinned laminae without excising the laminae. This technique enlarges the spinal canal. The purpose of this technique is to decompress the spinal cord and at the same time maintain clinical stability. Postoperative results were satisfactory without any major complication. Follow-up study was conducted in 78 cases with a minimal follow-up period of more than 2 years. Satisfactory clinical results were maintained for long periods postoperatively, and the enlargement of the spinal canal was well maintained as demonstrated on follow up X-ray study.

[A morphological study of the etiology and growth of ossification of the posterior longitudinal ligament of the spine].

To know causative and growth factors of ossification of the posterior longitudinal ligament (OPLL) of the spine, we carried out morphological investigation on 212 cases with OPLL and 9 cases of autopsies without OPLL. The results are as follows: 1) The etiology of OPLL ensued from enchondral ossification of ligamentous fibers has not only its primary source in a hereditary factor of polygenic character, but also anatomical stress, age and sex may be influential in causative factors. 2) When the degree of the hereditary factor is weak, the lesion initiates near the posterior border of the vertebral body and grow into a segmental or localized type of OPLL in the final form. When the degree of the hereditary factor is strong, a wide ossification of a continuous or mixed type of OPLL initiates all at once and grow up with movement of the spine, after which modeling continues to take place. 3) New ossification growth over time will arise from the stress resulting from movement of the spine.

[The choice of antibiotics for prophylaxis of postoperative infections in the field of orthopaedics. Clinical experience with cefoxitin].

The clinical effects of cefoxitin (CFX) were evaluated in the prophylaxis of postoperative infections in the field of orthopaedics. The clinical response was good in 46 out of 50 patients; an efficacy rate of 92%. Four patients (8%) who did not respond to CFX were suffering from infections due to Mycobacterium tuberculosis (1), suspected Pseudomonas aeruginosa (1), and infection of unknown organism (2). A review was also made of recent trends among clinically isolated bacterial strains and their susceptibility to antibiotics in the field of orthopaedics. CFX is recommended as an antibiotic of first choice for the prophylaxis of postoperative infections in the field of orthopaedics.