The association of spinal osteoarthritis with lumbar lordosis

<p>Abstract</p> <p>Background</p> <p>Careful review of published evidence has led to the postulate that the degree of lumbar lordosis may possibly influence the development and progression of spinal osteoarthritis, just as misalignment does in other joints. Spinal degeneration can ensue from the asymmetrical distribution of loads. The resultant lesions lead to a domino- like breakdown of the normal morphology, degenerative instability and deviation from the correct configuration. The aim of this study is to investigate whether a relationship exists between the sagittal alignment of the lumbar spine, as it is expressed by lordosis, and the presence of radiographic osteoarthritis.</p> <p>Methods</p> <p>112 female subjects, aged 40-72 years, were examined in the Outpatients Department of the Orthopedics' Clinic, University Hospital of Heraklion, Crete. Lumbar radiographs were examined on two separate occasions, independently, by two of the authors for the presence of osteoarthritis. Lordosis was measured from the top of L₁to the bottom of L₅as well as from the top of L₁to the top of S₁. Furthermore, the angle between the bottom of L₅to the top of S₁was also measured.</p> <p>Results and discussion</p> <p>49 women were diagnosed with radiographic osteoarthritis of the lumbar spine, while 63 women had no evidence of osteoarthritis and served as controls. The two groups were matched for age and body build, as it is expressed by BMI. No statistically significant differences were found in the lordotic angles between the two groups</p> <p>Conclusions</p> <p>There is no difference in lordosis between those affected with lumbar spine osteoarthritis and those who are disease free. It appears that osteoarthritis is not associated with the degree of lumbar lordosis.</p

Impaired Innate Immunity in Tlr4−/− Mice but Preserved CD8+ T Cell Responses against Trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or Myd88-Deficient Mice

The murine model of T. cruzi infection has provided compelling evidence that development of host resistance against intracellular protozoans critically depends on the activation of members of the Toll-like receptor (TLR) family via the MyD88 adaptor molecule. However, the possibility that TLR/MyD88 signaling pathways also control the induction of immunoprotective CD8+ T cell-mediated effector functions has not been investigated to date. We addressed this question by measuring the frequencies of IFN-γ secreting CD8+ T cells specific for H-2Kb-restricted immunodominant peptides as well as the in vivo Ag-specific cytotoxic response in infected animals that are deficient either in TLR2, TLR4, TLR9 or MyD88 signaling pathways. Strikingly, we found that T. cruzi-infected Tlr2−/−, Tlr4−/−, Tlr9−/− or Myd88−/− mice generated both specific cytotoxic responses and IFN-γ secreting CD8+ T cells at levels comparable to WT mice, although the frequency of IFN-γ+CD4+ cells was diminished in infected Myd88−/− mice. We also analyzed the efficiency of TLR4-driven immune responses against T. cruzi using TLR4-deficient mice on the C57BL genetic background (B6 and B10). Our studies demonstrated that TLR4 signaling is required for optimal production of IFN-γ, TNF-α and nitric oxide (NO) in the spleen of infected animals and, as a consequence, Tlr4−/− mice display higher parasitemia levels. Collectively, our results indicate that TLR4, as well as previously shown for TLR2, TLR9 and MyD88, contributes to the innate immune response and, consequently, resistance in the acute phase of infection, although each of these pathways is not individually essential for the generation of class I-restricted responses against T. cruzi