Ridge alterations following immediate implant placement and the treatment of bone defects with Bio-Oss in an animal model

Background: Conflicting data exist on the outcome of placing Bio‐Oss® (Geitslich Pharm AG, Wolhausen, Switzerland) into extraction sockets. It is therefore relevant to study whether the incorporation of Bio‐Oss into extraction sockets would influence bone healing outcome at the extraction sites. Purpose: The aim of this study was to assess peri‐implant bone changes when implants were placed in fresh extraction sockets and the remaining defects were filled with Bio‐Oss particles in a canine mandible model. Materials and Methods: Six mongrel dogs were used in the study. In one jaw quadrant of each animal, the fourth mandibular premolars were extracted with an elevation of the mucoperiosteal flap; implants were then placed in the fresh extraction sockets and the remaining defects were filled with Bio‐Oss particles. After 4 months of healing, micro‐computed tomography at the implant sites was performed. Osseointegration was calculated as the percent of implant surface in contact with bone. Additionally, bone height was measured in the peri‐implant bone. Results: Average osseointegration was 28.5% (ranged between 14.8 and 34.2%). The mean crestal bone loss was 4.7 ± 2.1 mm on the buccal aspect, 0.4 ± 0.5 mm on the mesial aspect, 0.4 ± 0.3 mm on the distal aspect, and 0.3 ± 0.4 mm on the lingual aspect. Conclusion: The findings from this study demonstrated that the placement of implants and Bio‐Oss® particles into fresh extraction sockets resulted in significant buccal bone loss with low osseointegration.     

Fusobacterium nucleatum GroEL induces risk factors of atherosclerosis in human microvascular endothelial cells and ApoE(-/-) mice

Infection and inflammation are risk factors in the initiation and progression of atherosclerosis. Periodontitis is one of the most prevalent chronic inflammations of the oral cavity, and has been reported to be associated with systemic disease. In this study, we evaluated whether the heat-shock protein GroEL of Fusobacterium nucleatum, one of the most prevalent bacteria in periodontitis, induces factors that predispose to atherosclerosis in human microvascular endothelial cells (HMEC-1) and apolipoprotein E-deficient (ApoE(-/-)) mice. GroEL induced the expression of chemokines such as monocyte chemoattractant protein-1 and interleukin-8 as well as cell adhesion molecules, such as intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E-selectin. GroEL induced the activity of tissue factor and reduced the activity of the tissue factor pathway inhibitor. Foam cell formation was induced by GroEL. GroEL-injected ApoE(-/-) mice showed significant atherosclerotic lesion progression compared with control mice. Serum levels of risk factors for atherosclerosis such as interleukin-6, C-reactive protein, and low-density lipoprotein were increased in GroEL-injected ApoE(-/-) mice compared with control mice, whereas serum levels of high-density lipoprotein were decreased. We could detect significantly higher levels of anti-F. nucleatum GroEL antibody in serum and F. nucleatum DNA in gingival crevicular fluid from patients with periodontitis than in that from healthy subjects. Our results indicate that the host response to the GroEL of periodontal pathogens like F. nucleatum may be a mechanism involved in atherosclerosis, supporting the association of periodontitis and systemic infection.     

Serum uric acid: a marker of metabolic syndrome and subclinical atherosclerosis in Korean men

Serum uric acid (SUA) is a potential risk factor for atherosclerosis. We assessed the relationship between SUA and subclinical atherosclerosis in Korean men (n = 3010). Multidetector computed tomography (MDCT) and ultrasonographic measurements of coronary artery calcification (CAC) and carotid intima-media thickness (cIMT), respectively, are markers of subclinical atherosclerosis. Odds ratios (ORs) of CAC score and cIMT across SUA levels were 1.101 (P = .046) and 1.266 (P = .002), respectively, after adjustment for several variables. The independent association between CAC and cIMT was observed (OR = 1.231, P < .001). Serum uric acid was independently associated with metabolic syndrome (MetS) with an OR of 1.415 (P < .001). Metabolic syndrome was only independently associated with cIMT, with an OR of 2.103 (P = .003). High-sensitivity C-reactive protein was positively correlated with SUA (r = .125, P < .001). Serum uric acid level is independently associated with CAC, cIMT, and MetS in Korean men.     

Phenotype diversity in type 1 Gaucher disease: discovering the genetic basis of Gaucher disease/hematologic malignancy phenotype by individual genome analysis

Gaucher disease (GD), an inherited macrophage glycosphingolipidosis, manifests with an extraordinary variety of phenotypes that show imperfect correlation with mutations in the GBA gene. In addition to the classic manifestations, patients suffer from increased susceptibility to hematologic and nonhematologic malignancies. The mechanism(s) underlying malignancy in GD is not known, but is postulated to be secondary to macrophage dysfunction and immune dysregulation arising from lysosomal accumulation of glucocerebroside. However, there is weak correlation between GD/cancer phenotype and the systemic burden of glucocerebroside-laden macrophages. Therefore, we hypothesized that genetic modifier(s) may underlie the GD/cancer phenotype. In the present study, the genetic basis of GD/T-cell acute lymphoblastic lymphoma in 2 affected siblings was deciphered through genomic analysis. GBA gene sequencing revealed homozygosity for a novel mutation, D137N. Whole-exome capture and massively parallel sequencing combined with homozygosity mapping identified a homozygous novel mutation in the MSH6 gene that leads to constitutional mismatch repair deficiency syndrome and increased cancer risk. Enzyme studies demonstrated that the D137N mutation in GBA is a pathogenic mutation, and immunohistochemistry confirmed the absence of the MSH6 protein. Therefore, precise phenotype annotation followed by individual genome analysis has the potential to identify genetic modifiers of GD, facilitate personalized management, and provide novel insights into disease pathophysiology.     

Cardiovascular manifestations of Takayasu arteritis and their relationship to the disease activity: analysis of 204 Korean patients at a single center

Takayasu's arteritis (TA) is primary vasculitis. Cardiac involvements in TA is due to the consequences of the vascular lesions as well as the primary pathology of the heart. The disease activity of TA is known to influence the prognosis of TA. We hypothesized that the cardiovascular involvement of TA is related to the disease activity. We evaluated the cardiovascular manifestations of TA, and we assessed their relation to the disease activity of TA. Two hundred four patients were diagnosed with TA from September, 1994 to March, 2009 according to the diagnostic criteria of the 1990 American College of Rheumatology. Their clinical features and the laboratory, angiographic and echocardiographic findings were retrospectively reviewed. The group with active disease activity was defined as satisfying one of the following criteria: i) an elevated ESR or CRP level, ii) thickened arterial wall with mural enhancement on CT or MR angiography, and iii) carotidynia at the time of the initial diagnosis. One hundred thirty nine patients (69.2%) were classified as the active group. The cardiovascular signs and symptoms were not generally different between the active and inactive groups. The active TA patients had more frequent involvement of the ascending aorta and the aortic arch and its main branches than did the inactive group. The active group showed a higher incidence of significant aortic valve regurgitation and pulmonary hypertension, and a higher level of NT-proBNP. These findings suggest that disease activity plays an important role for the cardiovascular manifestations of TA. The TA patients with higher activity have more cardiovascular morbidity compared to the TA patients with low disease activity.