907 resultados para Cement-loaded, Kuntscher Nail, Revision, Hip Arthroplasty, Bone Loss


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Dimensional alterations of the facial bone wall following tooth extractions in the esthetic zone have a profound effect on treatment outcomes. This prospective study in 39 patients is the first to investigate three-dimensional (3D) alterations of facial bone in the esthetic zone during the initial 8 wks following flapless tooth extraction. A novel 3D analysis was carried out, based on 2 consecutive cone beam computed tomographies (CBCTs). A risk zone for significant bone resorption was identified in central areas, whereas proximal areas yielded only minor changes. Correlation analysis identified a facial bone wall thickness of ≤ 1 mm as a critical factor associated with the extent of bone resorption. Thin-wall phenotypes displayed pronounced vertical bone resorption, with a median bone loss of 7.5 mm, as compared with thick-wall phenotypes, which decreased by only 1.1 mm. For the first time, 3D analysis has allowed for documentation of dimensional alterations of the facial bone wall in the esthetic zone of humans following extraction. It also characterized a risk zone prone to pronounced bone resorption in thin-wall phenotypes. Vertical bone loss was 3.5 times more severe than findings reported in the existing literature.

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OBJECTIVE Recent review articles have shown that open debridement is more effective in the treatment of peri-implantitis than closed therapy. However, surgery may result in marginal recession and compromise esthetics. The purpose of this study was to assess the efficacy of nonsurgical antimicrobial photodynamic therapy (aPDT) in moderate vs severe defects. METHOD AND MATERIALS The study encompassed 16 patients with a total of 18 ailing implants. Ten of these implants showed moderate bone loss (< 5 mm; Group 1) and eight implants severe defects (5 through 8 mm; Group 2). All implants received aPDT without surgical intervention. At baseline and 2 weeks, 3 months, and 6 months after therapy, peri-implant health was assessed including sulcus bleeding index (SBI), probing depth (PD), distance from implant shoulder to marginal mucosa (DIM), and clinical attachment level (CAL). Radiographic evaluation of distance from implant to bone (DIB) allowed comparison of peri-implant hard tissues after 6 months. RESULTS Baseline values for SBI were comparable in both groups. Three months after therapy, in both groups, SBI and CAL decreased significantly. In contrast, after 6 months, CAL and DIB increased significantly in Group 2, not in Group 1. However, DIM-values were not statistically different 6 months after therapy in both groups. CONCLUSION Within the limits of this 6-month study, nonsurgical aPDT could stop bone resorption in moderate peri-implant defects but not in severe defects. However, marginal tissue recession was not significantly different in both groups at the end of the study. Therefore, especially in esthetically important sites, surgical treatment of severe peri-implantitis defects seems to remain mandatory.

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OBJECTIVE: The objective of the study is to compare the clinical, microbiological and host-derived effects in the non-surgical treatment of initial peri-implantitis with either adjunctive local drug delivery (LDD) or adjunctive photodynamic therapy (PDT) after 12 months. MATERIALS AND METHODS: Forty subjects with initial peri-implantitis, that is, pocket probing depths (PPD) 4-6 mm with bleeding on probing (BoP) and radiographic bone loss ≤2 mm, were randomly assigned to two treatment groups. All implants were mechanically debrided with titanium curettes and with a glycine-based powder airpolishing system. Implants in the test group (N = 20) received adjunctive PDT, whereas minocycline microspheres were locally delivered into the peri-implant pockets of control implants (N = 20). At sites with residual BoP, treatment was repeated after 3, 6, 9 and 12 months. The primary outcome variable was the change in the number of peri-implant sites with BoP. Secondary outcome variables included changes in PPD, clinical attachment level (CAL), mucosal recession (REC) and in bacterial counts and crevicular fluid (CF) levels of host-derived biomarkers. RESULTS: After 12 months, the number of BoP-positive sites decreased statistically significantly (P < 0.05) from baseline in both groups (PDT: 4.03 ± 1.66-1.74 ± 1.37, LDD: 4.41 ± 1.47-1.55 ± 1.26). A statistically significant (P < 0.05) decrease in PPD from baseline was observed at PDT-treated sites up to 9 months (4.19 ± 0.55 mm to 3.89 ± 0.68 mm) and up to 12 months at LDD-treated sites (4.39 ± 0.77 mm to 3.83 ± 0.85 mm). Counts of Porphyromonas gingivalis and Tannerella forsythia decreased statistically significantly (P < 0.05) from baseline to 6 months in the PDT and to 12 months in the LDD group, respectively. CF levels of IL-1β decreased statistically significantly (P < 0.05) from baseline to 12 months in both groups. No statistically significant differences (P > 0.05) were observed between groups after 12 months with respect to clinical, microbiological and host-derived parameters. CONCLUSIONS: Non-surgical mechanical debridement with adjunctive PDT was equally effective in the reduction of mucosal inflammation as with adjunctive delivery of minocycline microspheres up to 12 months. Adjunctive PDT may represent an alternative approach to LDD in the non-surgical treatment of initial peri-implantitis.

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BACKGROUND Due to the increasing number of older people, there is a need for studies focused on this population. The aims of the present study are to assess oral and systemic conditions in individuals aged 60 to 95 years with access to dental insurance. METHODS Probing depths (PDs), tooth loss, alveolar bone levels, and systemic health were studied among a representative cohort of older individuals. RESULTS A total of 1,147 individuals in young-old (aged 60 or 67 years), old (aged 72 or 78 years), and old-old (aged ≥81 years) age groups were enrolled, including 200 individuals who were edentulous, in this study. Annual dental care was received by 82% of dentate individuals. Systemic diseases were common (diabetes: 5.8%; cardiovascular diseases: 20.7%; obesity: 71.2%; elevated C-reactive protein [CRP]: 98.4%). Serum CRP values were unrelated to periodontal conditions. Rates of periodontitis, defined as ≥30% of sites with a distance from cemento-enamel junction to bone of ≥5 mm, were 11.2% in women in the young-old age group and 44.9% in men in the old-old age group. Individuals in older age groups had a higher likelihood of periodontitis defined by bone loss and cutoff levels of PD ≥5 mm (odds ratio: 1.8; 95% confidence interval: 1.2 to 2.5; P <0.01). A total of 7% of individuals in the old-old age group had ≥20 teeth and no periodontitis. Systemic diseases, dental use, or smoking were not explanatory, whereas age and sex were explanatory for periodontitis. CONCLUSIONS The prevalence of periodontitis increased with age. Sex seems to be the dominant explanatory factor for periodontitis in older individuals. Despite frequent dental visits, overall oral health in the oldest age cohort was poor.

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BACKGROUND Survival rates in implant dentistry today are high, although late failures do occur for many reasons, including peri-implant infections. The primary objective of this study is to investigate microbiota around single turned implants after 16 to 22 years. Secondary objectives are to compare teeth and implants and to correlate microbiologic, radiographic, and clinical parameters. METHODS A total of 46 patients with single implants were invited for a clinical examination. Clinical data were collected from implants and contralateral natural teeth. Radiographic bone level was measured around implants. Microbiologic samples were taken from implants, contralateral teeth, and the deepest pocket per quadrant. Samples were analyzed with DNA-DNA hybridization including 40 species. Statistical analysis was performed using Wilcoxon signed-rank tests, McNemar tests, and Spearman correlation coefficients with a 0.05 significance level. RESULTS Mean follow-up was 18.5 years (range 16 to 22 years). Tannerella forsythia (1.5 × 10(5)) and Veillonella parvula (1.02 × 10(5)) showed the highest concentrations around implants and teeth, respectively. Porphyromonas gingivalis, Prevotella intermedia, and T. forsythia were significantly more present around implants than teeth. Mean counts were significantly higher around implants than teeth for Parvimonas micra, P. gingivalis, P. intermedia, T. forsythia, and Treponema denticola. Total DNA count was correlated to interproximal bleeding index (r = 0.409) and interproximal probing depth (r = 0.307). No correlations were present with plaque index or radiographic bone level. CONCLUSIONS In the present study, bacterial counts around single implants in periodontally healthy patients are rather low. Although pathogenic bacteria are present, some in higher numbers around implants than teeth (five of 40), the majority of implants present with healthy peri-implant tissues without progressive bone loss.

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PURPOSE In patients with hormone-dependent postmenopausal breast cancer, standard adjuvant therapy involves 5 years of the nonsteroidal aromatase inhibitors anastrozole and letrozole. The steroidal inhibitor exemestane is partially non-cross-resistant with nonsteroidal aromatase inhibitors and is a mild androgen and could prove superior to anastrozole regarding efficacy and toxicity, specifically with less bone loss. PATIENTS AND METHODS We designed an open-label, randomized, phase III trial of 5 years of exemestane versus anastrozole with a two-sided test of superiority to detect a 2.4% improvement with exemestane in 5-year event-free survival (EFS). Secondary objectives included assessment of overall survival, distant disease-free survival, incidence of contralateral new primary breast cancer, and safety. RESULTS In the study, 7,576 women (median age, 64.1 years) were enrolled. At median follow-up of 4.1 years, 4-year EFS was 91% for exemestane and 91.2% for anastrozole (stratified hazard ratio, 1.02; 95% CI, 0.87 to 1.18; P = .85). Overall, distant disease-free survival and disease-specific survival were also similar. In all, 31.6% of patients discontinued treatment as a result of adverse effects, concomitant disease, or study refusal. Osteoporosis/osteopenia, hypertriglyceridemia, vaginal bleeding, and hypercholesterolemia were less frequent on exemestane, whereas mild liver function abnormalities and rare episodes of atrial fibrillation were less frequent on anastrozole. Vasomotor and musculoskeletal symptoms were similar between arms. CONCLUSION This first comparison of steroidal and nonsteroidal classes of aromatase inhibitors showed neither to be superior in terms of breast cancer outcomes as 5-year initial adjuvant therapy for postmenopausal breast cancer by two-way test. Less toxicity on bone is compatible with one hypothesis behind MA.27 but requires confirmation. Exemestane should be considered another option as up-front adjuvant therapy for postmenopausal hormone receptor-positive breast cancer.

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AIM We investigated the association between angiographically verified coronary artery disease (CAD) and subgingival Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola. MATERIALS AND METHODS The cross-sectional study population (n = 445) comprised 171 (38.4%) patients with Stable CAD, 158 (35.5%) with acute coronary syndrome (ACS) and 116 (26.1%) with no significant CAD (No CAD). All patients participated in clinical and radiological oral health examinations. Pooled subgingival bacterial samples were analysed by checkerboard DNA-DNA hybridization assays. RESULTS In all study groups, the presence of P. gingivalis, T. forsythia and T. denticola indicated a significant (p ≤ 0.001) linear association with the extent of alveolar bone loss (ABL), but A. actinomycetemcomitans did not (p = 0.074). With a threshold level of bacterial cells 1 × 10(5) A. actinomycetemcomitans was significantly more prevalent in the Stable CAD group (42.1%) compared to the No CAD group (30.2%) (p = 0.040). In a multi-adjusted logistic regression analysis using this threshold, A. actinomycetemcomitans positivity associated with Stable CAD (OR 1.83, 95% CI 1.00-3.35, p = 0.049), but its level or levels of other bacteria did not. CONCLUSIONS The presence of subgingival A. actinomycetemcomitans associates with an almost twofold risk of Stable CAD independently of alveolar bone loss.

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AIM The aim of this prospective, randomized, controlled multicenter study was to determine the 3-year efficacy and stability of the soft and hard tissues at implants with a different geometry that were placed in fresh extraction sockets. MATERIAL AND METHODS Implants with two different configurations, cylindrical (Group A) or conical/cylindrical (Group B) were installed, and healing abutments were attached. Sixteen weeks after implant placement, subjects returned for a re-entry procedure. Prosthetic restorations were delivered 22 weeks after implant placement. Each subject was placed in a 3-year follow-up program, including examinations at yearly visits including various soft tissue and bone level parameters. RESULTS The percentage of sites that were considered inflamed during the follow-up period was stable and varied between 8.8% and 10.2%. The radiographic examinations documented improved bone levels at the final examination and the mean improvement from baseline (placement of permanent restoration; PR) amounted to 0.17 ± 0.67 mm. More than 70% (54 of 76) of the implants monitored in this study suffered no bone loss during the maintenance period. Moreover, there was an obvious "gain" of interproximal soft tissue volume and at the 3-year examination around 25% of all embrasure gaps were completely filled with "papillae". CONCLUSIONS Both conical/cylindrical and cylindrical implants placed in fresh extraction sockets allowed proper soft and hard tissue healing to occur. At both types of implants, mucosal inflammation was infrequent, marginal bone levels were maintained, and soft tissue volume increased gradually after the placement of the permanent restoration.

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AIM To assess the clinical and radiographic outcomes applying a combined resective and regenerative approach in the treatment of peri-implantitis. MATERIALS AND METHODS Subjects with implants diagnosed with peri-implantitis (i.e., pocket probing depth (PPD) ≥5 mm with concomitant bleeding on probing (BoP) and ≥2 mm of marginal bone loss or exposure of ≥1 implant thread) were treated by means of a combined approach including the application of a deproteinized bovine bone mineral and a collagen membrane in the intrabony and implantoplasty in the suprabony component of the peri-implant lesion, respectively. The soft tissues were apically repositioned allowing for a non-submerged healing. Clinical and radiographic parameters were evaluated at baseline and 12 months after treatment. RESULTS Eleven subjects with 11 implants were treated and completed the 12-month follow-up. No implant was lost yielding a 100% survival rate. At baseline, the mean PPD and mean clinical attachment level (CAL) were 8.1 ± 1.8 mm and 9.7 ± 2.5 mm, respectively. After 1 year, a mean PPD of 4.0 ± 1.3 mm and a mean CAL of 6.7 ± 2.5 mm were assessed. The differences between the baseline and the follow-up examinations were statistically significant (P = 0.001). The mucosal recession increased from 1.7 ± 1.5 at baseline to 3.0 ± 1.8 mm at the 12-month follow-up (P = 0.003). The mean% of sites with BoP+ around the selected implants decreased from 19.7 ± 40.1 at baseline to 6.1 ± 24.0 after 12 months (P = 0.032). The radiographic marginal bone level decreased from 8.0 ± 3.7 mm at baseline to 5.2 ± 2.2 mm at the 12-month follow-up (P = 0.000001). The radiographic fill of the intrabony component of the defect amounted to 93.3 ± 13.0%. CONCLUSION Within the limits of this study, a combined regenerative and resective approach for the treatment of peri-implant defects yielded positive outcomes in terms of PPD reduction and radiographic defect fill after 12 months.

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Owing to its single surgical intervention, immediate implant placement has the advantage of shortening treatment time, and thus positively affects patient morbidity. According to the bone resorption pattern after tooth extraction, bone loss should be anticipated if immediate implant placement is considered. The present case report aims to present a possible treatment option and to demonstrate that a partially edentulous arch may be rehabilitated esthetically by immediate implant placement and by corresponding anticipatory measures.

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A tightly attached keratinized mucosa around endosseous dental implants is believed to be protective against peri-implant bone loss. Tension caused by buccal frena and mobile non keratinized mucosa is to avoid. This case report documents the optimization of peri-implant mucosal conditions in the upper and lower jaw. At the time of second stage surgery (re-entry) at submucosally osseointegrated dental implants an enlargement of keratinized mucosa and a thickening of soft tissue was obtained administrating a vestibuloplasty combined by a free gingival graft or a vestibuloplasty combined by an apically moved flap.

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Rebound-associated vertebral fractures may follow treatment discontinuation of highly potent reversible bone antiresorptives, resulting from the synergy of rapid bone resorption and accelerated microdamage accumulation in trabecular bone. INTRODUCTION The purposes of this study are to characterize rebound-associated vertebral fractures following the discontinuation of a highly potent reversible antiresorptive therapy based on clinical observation and propose a pathophysiological rationale. METHODS This study is a case report of multiple vertebral fractures early after discontinuation of denosumab therapy in a patient with hormone receptor-positive non-metastatic breast cancer treated with an aromatase inhibitor. RESULTS Discontinuation of highly potent reversible bone antiresorptives such as denosumab may expose patients to an increased fracture risk due to the joined effects of absent microdamage repair during therapy followed by synchronous excess activation of multiple bone remodelling units at the time of loss-of-effect. We suggest the term rebound-associated vertebral fractures (RVF) for this phenomenon characterized by the presence of multiple new clinical vertebral fractures, associated with either no or low trauma, in a context consistent with the presence of high bone turnover and rapid loss of lumbar spine bone mineral density (BMD) occurring within 3 to 12 months after discontinuation (loss-of-effect) of a reversible antiresorptive therapy in the absence of secondary causes of bone loss or fractures. Unlike atypical femoral fractures that emerge from failure of microdamage repair in cortical bone with long-term antiresorptive treatment, RVF originate from the synergy of rapid bone resorption and accelerated microdamage accumulation in trabecular bone triggered by the discontinuation of highly potent reversible antiresorptives. CONCLUSIONS Studies are urgently needed to i) prove the underlying pathophysiological processes suggested above, ii) establish the predictive criteria exposing patients to an increased risk of RVF, and iii) determine appropriate treatment regimens to be applied in such patients.

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OBJECTIVE To investigate the regulatory effect of tumour necrosis factor (TNF) blockade with infliximab on the distribution of peripheral blood monocyte subpopulations in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). METHODS Purified CD11b+CD14+ monocytes from 5 patients with RA and 5 AS were analysed ex vivo before and after infliximab treatment by flow cytometry for CD16, CD163, CD11b, C-C chemokine receptor type 2 (CCR2) and CXC chemokine receptor 4 (CXCR4) at baseline and at days 2, 14, 84 and 168 after the first infliximab administration. Serum levels of the stromal cell-derived factor (SDF)-1 and monocyte chemotactic peptide (MCP)-1 at different time points were measured in either patient group before and on infliximab treatment. RESULTS Anti-TNF treatment with infliximab led to a significant increase of circulating CD11b+ non-classical and a concomitantly decrease of CD11b+ classical monocytes, to a decline in SDF-1 levels and reduced expression of CCR2 and CXCR4 on non-classical monocyte subpopulation. CONCLUSIONS Our study shows, that TNFα blockade by infliximab resulted in a dichotomy of the regulation of classical and non-classical monocytes that might have substantial impact on inhibition of osteoclastogenesis and of subsequent juxta-articular bone destruction and systemic bone loss in RA and AS.

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IL-4 is a pleiotropic immune cytokine secreted by activated TH2 cells that inhibits bone resorption both in vitro and in vivo. The cellular targets of IL-4 action as well as its intracellular mechanism of action remain to be determined. We show here that IL-4 inhibits receptor activator of NF-κB ligand-induced osteoclast differentiation through an action on osteoclast precursors that is independent of stromal cells. Interestingly, this inhibitory effect can be mimicked by both natural as well as synthetic peroxisome proliferator-activated receptor γ1 (PPARγ1) ligands and can be blocked by the irreversible PPARγ antagonist GW 9662. These findings suggest that the actions of IL-4 on osteoclast differentiation are mediated by PPARγ1, an interpretation strengthened by the observation that IL-4 can activate a PPARγ1-sensitive luciferase reporter gene in RAW264.7 cells. We also show that inhibitors of enzymes such as 12/15-lipoxygenase and the cyclooxygenases that produce known PPARγ1 ligands do not abrogate the IL-4 effect. These findings, together with the observation that bone marrow cells from 12/15-lipoxygenase-deficient mice retain sensitivity to IL-4, suggest that the cytokine may induce novel PPARγ1 ligands. Our results reveal that PPARγ1 plays an important role in the suppression of osteoclast formation by IL-4 and may explain the beneficial effects of the thiazolidinedione class of PPARγ1 ligands on bone loss in diabetic patients.

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A doença periodontal (DP) corresponde a um grupo de doenças inflamatórias que acomete as estruturas periodontais de proteção e de suporte e pode levar à perda dentária. A etiologia está relacionada à placa dentobacteriana que leva à produção de grande quantidade de citocinas pró-inflamatórias importantes na destruição tecidual. A angiotensina (Ang) II também pode contribuir para a inflamação e destruição tecidual no periodonto agindo como mediador chave. A utilização de drogas que atuem na cascata do sistema renina-angiotensina (SRA) poderia interferir no estado de saúde ou inflamação do tecido mole, na perda óssea alveolar e na expressão gênica dos componentes do SRA e mediadores inflamatórios. Portanto, o objetivo do presente trabalho foi investigar se o ramipril, um inibidor da enzima conversora de angiotensina (ECA), altera a progressão da DP induzida experimentalmente em ratos. Foi utilizado o modelo de indução da DP por colocação de ligadura ao redor do primeiro molar inferior direito de ratos. Os grupos com 10 animais cada, foram divididos em tratados com ramipril (via gavagem 10 mg/kg/dia) ou água (veículo) durante 14 e 21 dias e o grupo Sham submetido à indução fictícia da DP. Outros quatro grupos foram submetidos ao pré-tratamento com ramipril durante os períodos de 7 e 14 dias e após a indução da DP e tratados por 14 ou 21 dias. As metodologias de avaliação foram: extração de RNA total, transcrição reversa seguida de reação em cadeia da polimerase quantitativa (RTqPCR), análises histológica e da perda óssea alveolar. Os dados foram analisados por meio de gráficos e os resultados foram submetidos à análise unidirecional de variância (ANOVA) e representaram médias e respectivos desvios-padrão. Diferenças entre os grupos foram consideradas estatisticamente significativas quando p < 0,05. Com base nos resultados obtidos pode-se concluir que o ramipril foi capaz de reduzir a progressão da perda óssea no grupo tratado por 21 dias (DP-21d-Rami), entretanto houve aumento do processo inflamatório, além de alteração da expressão de RNAm de ECA-2 e do receptor Mas, alguns mediadores do processo inflamatório, como COX2 e VEGF, e os receptores VEGF-R1 e VEGF-R2.