Changes in Bone Mineral Density of Both Proximal Femurs after Total Knee Arthroplasty

Background

This study investigated the effects of total knee arthroplasty (TKA) on bone mineral density (BMD) of the proximal femur in patients who underwent the procedure.

Methods

Forty-eight patients scheduled to undergo unilateral TKA because of primary knee osteoarthritis were included in this study, which was conducted at a medical center between October 2006 and October 2009. In these 48 patients, 96 hips were evaluated. Measurement of BMD was performed preoperatively and one month, three months, six months, and one year after unilateral TKA. Repeated measured analysis of variance and paired t-tests for comparison of two repeated samples were used to compare differences between time points (preoperation, one, three, six, and 12 months) and between the operative and nonoperative sides.

Results

Preoperatively, BMD of the femoral neck, trochanter, and total hip on the operative side were lower than on the nonoperative side; however, there was no statistical difference. BMD of both femoral neck areas was significantly lower than preoperative BMD at one month and three months after TKA. BMD of both trochanter areas was significantly lower than preoperative BMD at one month and three months after TKA. BMD of both total hips was significantly lower than preoperative BMD at three months after TKA. However, no statistical differences of changes in BMD were observed between the operative and nonoperative sides at each measurement time.

Conclusions

According to our results, TKA was found to affect both proximal femurs during the acute period. However, TKA did not affect a change in BMD of the proximal femur during one year postoperative.     

Enhancement of antigen-specific CD8 T cell responses by co-delivery of Fc-fused CXCL11

Chemokines have been known to play an important role in eliciting adaptive immune responses by, selectively attracting the innate cellular components to the site of antigen presentation. In this study, we demonstrated that all three CXCR3 ligands, CXCL9, CXCL10, and CXCL11, could act as a strong, genetic adjuvant. Among them, CXCL11 increased vaccine antigen-specific CD8 T cells, including, several cytokine secretions (IFN-γ and TNF-α) to a greater degree than the other two CXCR3 ligands. Fc-fusion of CXCL11 (CXCL11-Fc) induced similar but slightly higher CD8 T cell response, which, appeared to be antigen- (ovalbumin (OVA) vs. human papillomavirus 16 (HPV16) E7) and vaccine, type- (adenovirus vs. DNA vaccine) independent. In addition, the adjuvant effect of CXCL11-Fc was, further confirmed by suppressing tumor growth and extension of survival rates in a therapeutic tumor, model, which was correlated with enhanced antigen-specific CD8 T cell responses. Interestingly, the, enhanced antigen-specific CD8 T cell responses by co-delivery of CXCL11-Fc were associated with CD8, T cell proliferation, followed by increased total and effector memory T cell frequencies. Taken together, our findings provide a novel role of CXCL11 as a strong genetic adjuvant which might be used to, increase antigen-specific CD8 T cell immunity elicited by vaccination.     

Chemically induced Salmonella enteritidis ghosts as a novel vaccine candidate against virulent challenge in a rat model

Salmonella enteritidis ghosts (SEGs), non-living empty bacterial cell envelopes were generated by using the minimum inhibitory concentration (MIC) of sodium hydroxide (NaOH) and investigated as a vaccine candidate in rats. To determine the immunogenicity and protective efficacy of SEG vaccine, rats were divided into four groups: group A (non-vaccinated control), group B (orally vaccinated), group C (intramuscularly vaccinated) and group D (intramuscularly vaccinated with complete Freund's adjuvant). Vaccination of rats with SEGs induced significant immune responses before and after virulent challenge. Rats vaccinated with SEGs showed significant increases in serum IgG antibodies after challenging with virulent S. enteritidis on week 8 and week 10 (P < 0.01). During the vaccination period, groups B, C and D showed significantly higher serum bactericidal activity (SBA) compared to group A (P < 0.01). Most importantly, bacterial loads in vaccinated groups were significantly lower than in the non-vaccinated group (P < 0.01). In conclusion, these results show that the chemically induced SEGs as a vaccine candidate against virulent challenge.     

Motor intentional disorders in vascular mild cognitive impairment and vascular dementia of subcortical type

Subcortical vascular mild cognitive impairment (svMCI), a prodromal stage of subcortical vascular dementia (SVaD), is primarily associated with frontal injuries, whereas amnestic MCI (aMCI) is associated with temporoparietal injuries. Twenty-seven patients with svMCI, 20 with aMCI, 14 with SVaD, and 10 normal controls underwent motor intentional tasks (force initiation, development, maintenance, and termination) using a force dynamometer. Of the four motor intentional tasks, the maintenance task proved sensitive in differentiating svMCI from aMCI. In most motor intentional tasks, performances of svMCI patients were intermediate between those of controls and SVaD patients (initiation and termination: NC=aMCI=svMCI>SVaD; development: NC>aMCI=svMCI>SVaD; maintenance: NC=aMCI>svMCI=SVaD).     

Lipocalin-2 deficiency attenuates neuroinflammation and brain injury after transient middle cerebral artery occlusion in mice

Lipocalin-2 (LCN2) is a secreted protein of the lipocalin family, but little is known about the expression or the role of LCN2 in the central nervous system. Here, we investigated the role of LCN2 in ischemic stroke using a rodent model of transient cerebral ischemia. Lipocalin-2 expression was highly induced in the ischemic brain and peaked at 24 hours after reperfusion. After transient middle cerebral artery occlusion, LCN2 was predominantly expressed in astrocytes and endothelial cells, whereas its receptor (24p3R) was mainly detected in neurons, astrocytes, and endothelial cells. Brain infarct volumes, neurologic scores, blood–brain barrier (BBB) permeabilities, glial activation, and inflammatory mediator expression were significantly lower in LCN2-deficient mice than in wild-type animals. Lipocalin-2 deficiency also attenuated glial neurotoxicity in astrocyte/neuron cocultures after oxygen-glucose deprivation. Our results indicate LCN2 has a critical role in brain injury after ischemia/reperfusion, and that LCN2 may contribute to neuronal cell death in the ischemic brain by promoting neurotoxic glial activation, neuroinflammation, and BBB disruption.     

Wnt Signaling Regulates Pulp Volume and Dentin Thickness

Odontoblasts, cementoblasts, ameloblasts, and osteoblasts all form mineralized tissues in the craniofacial complex, and all these cell types exhibit active Wnt signaling during postnatal life. We set out to understand the functions of this Wnt signaling, by evaluating the phenotypes of mice in which the essential Wnt chaperone protein, Wntless was eliminated. The deletion of Wls was restricted to cells expressing Osteocalcin (OCN), which in addition to osteoblasts includes odontoblasts, cementoblasts, and ameloblasts. Dentin, cementum, enamel, and bone all formed in OCN‐Cre;Wls^fl/fl mice but their homeostasis was dramatically affected. The most notable feature was a significant increase in dentin volume and density. We attribute this gain in dentin volume to a Wnt‐mediated misregulation of Runx2. Normally, Wnt signaling stimulates Runx2, which in turn inhibits dentin sialoprotein (DSP); this inhibition must be relieved for odontoblasts to differentiate. In OCN‐Cre;Wls^fl/fl mice, Wnt pathway activation is reduced and Runx2 levels decline. The Runx2‐mediated repression of DSP is relieved and odontoblast differentiation is accordingly enhanced. This study demonstrates the importance of Wnt signaling in the homeostasis of mineralized tissues of the craniofacial complex. © 2014 American Society for Bone and Mineral Research.