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New Advances and Potentials for Treatment of Ankylosing Spondylitis
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New Advances and Potentials for Treatment of Ankylosing Spondylitis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: closed (20 June 2021) | Viewed by 1861

Special Issue Editor

Prof. Dr. Carlos Lopez-Larrea

E-Mail Website
Guest Editor
Immunology Department, Hospital Universitario Central de Asturias (HUCA), Translational Immunology Laboratory, Health Research Institute of the Principality of Asturias (ISPA), 33011 Oviedo, Spain
Interests: Spondyltis (AS) and spondyloarthritis (SpA); HLA-B27 and ERAP1/2; functional genomics; IL-23–IL-17 pathway; TNF-alpha; Janus kinases (JAK1/STATs) signaling; gut micobiota; immune regulation of bone; immune-metabolism; epigenetic regulation

Special Issue Information

Dear Colleagues,

Ankylosing spondylitis (AS) is a chronic autoinflammatory disease affecting the axial skeleton. HLA-B27 is the major genetic factor (MHC-I) that confers susceptibility to AS. Other genetic factors, through genome-wide association studies (GWAS), have been described in AS, being relevant to the contribution of the aminopeptidase ERAP1 that plays a role in epistasis with HLA-B27. Remarkably, the other genes which were found to be related to immune and inflammatory response were the TNF-alpha and the IL-23/Th17 axis. Therapeutic agents targeting these inflammatory pathways have proven to be successful in suppressing many of the clinical symptoms and signs of AS. Other inflammatory cytokine signals related with Janus kinases (JAKs/Tyk2 and STATs) signaling are targets for immunomodulation. Moreover, immune-metabolism and epigenetics, which change in chromatin dynamics (as p300, BET proteins), could contribute to these inflammatory processes, opening a new pathway for therapeutic intervention. In addition, dysbiosis in the gut of AS patients has been described, opening the use in therapeutics and personalized medicine. However, despite these findings, there are not yet any treatments that have been shown to robustly slow the rate of ankylosis. This is a critical point that needs to be explored in depth. This review will be address these pathways, integrating their functional interplay in AS for a better understanding of disease pathogenesis and the development of an innovative therapeutic approach.

Prof. Dr. Carlos Lopez-Larrea
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • spondyltis (AS) and spondyloarthritis (SpA)
  • HLA-B27 and ERAP1/2
  • functional genomics
  • IL-23–IL-17 pathway
  • TNF-alpha
  • Janus kinases (JAK1/STATs) signaling
  • gut microbiota
  • immune regulation of bone
  • immune-metabolism
  • epigenetic regulation

Published Papers (1 paper)

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Research

11 pages, 805 KiB  
Article
Prevalence and Associated Factors of Low Bone Mineral Density in the Femoral Neck and Total Hip in Axial Spondyloarthritis: Data from the CASTRO Cohort
by Laura Bautista-Aguilar, Clementina López-Medina, Lourdes Ladehesa-Pineda, María del Carmen Ábalos-Aguilera, Desirée Ruiz-Vilchez, Juan Luis Garrido-Castro, Ignacio Gómez-García, María Ángeles Puche-Larrubia, Asunción Salmoral-Chamizo, Eduardo Collantes-Estévez, Alejandro Escudero-Contreras and Pilar Font-Ugalde
J. Clin. Med. 2021, 10(12), 2664; https://doi.org/10.3390/jcm10122664 - 17 Jun 2021
Cited by 1 | Viewed by 1501
Abstract
Studies on osteoporosis in axial spondyloarthritis (axSpA) have focused on the lumbar segment, and few studies have assessed bone mineral density (BMD) in the hip and femoral neck in these patients. The aim of this study was to evaluate the prevalence of low [...] Read more.
Studies on osteoporosis in axial spondyloarthritis (axSpA) have focused on the lumbar segment, and few studies have assessed bone mineral density (BMD) in the hip and femoral neck in these patients. The aim of this study was to evaluate the prevalence of low BMD and osteopenia in the total hip or femoral neck and the factors associated with these conditions in axSpA patients. This was a single-centre, observational, cross-sectional study among consecutive patients with axSpA according to the ASAS criteria from the CASTRO registry. All patients underwent total hip and femoral neck DXA BMD measurements. Low BMD was defined as a Z-score less than −1, and osteopenia was defined as a T-score less than −1. Multivariate logistic and generalised linear regressions were used to evaluate factors independently associated with low BMD and osteopenia in the hip or femoral neck and those associated with variability in BMD, respectively. A total of 117 patients were included, among which 30.8% were female and the mean age was 45 years. A total of 36.0% of patients had low BMD (28.1% in the total hip and 27.4% in the femoral neck), and 56.0% of patients had osteopenia (44.7% in the total hip and 53.8% in the femoral neck). A multivariate logistic regression showed that age, radiographic sacroiliitis and ASAS-HI were independently associated with low BMD in the total hip or femoral neck. Factors that were independently associated with osteopenia were Body Mass Index, disease duration, radiographic sacroiliitis and ASAS-HI. In conclusion, 36% of the patients with axSpA had low BMD in the total hip or femoral neck. A younger age and radiographic sacroiliitis were the most important factors associated with decreased BMD. Full article
(This article belongs to the Special Issue New Advances and Potentials for Treatment of Ankylosing Spondylitis)
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