Advances in the Molecular Mechanisms of Inflammatory Arthritis and Inflammation-Related Bone Changes: 2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 1 November 2026 | Viewed by 912

Special Issue Editor

Special Issue Information

Dear Colleagues,

This Special Issue aims to summarise advances in the molecular mechanisms of inflammatory processes leading to arthritis and bone changes, and thus focuses on both the immunological and the osteological organ system. Advances in autoimmunity and auto-inflammation as well as advances in our knowledge of bone loss and bone growth are welcome for this Special Issue. In addition, osteo-immunological aspects describing the interactions between the immunological and the osteological systems are encouraged, as are studies on the intracellular, cellular and in vivo levels. The knowledge about such molecular mechanisms will provide new stimuli for further clinical research, including new treatment options for inflammatory arthritis in the acute and the chronic disease-phases and immune-related problems after prosthetic or other bone surgery.

Prof. Carlo Perricone
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 250 words) can be sent to the Editorial Office for assessment.

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. Biomolecules is an international peer-reviewed open access monthly 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 2700 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

  • inflammatory arthritis
  • molecular mechanisms
  • bone changes
  • osteoimmunology
  • autoimmunity

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

18 pages, 4816 KB  
Article
Lactate-Driven Reprogramming of Monocyte Bridges Bone Loss in Inflammatory Comorbidities
by Junbin Wei, Zhiqian Ye, Deqian Tang, Manqing Liu, Botian Tan, Houze Li, Yan Li and Qianmin Ou
Biomolecules 2026, 16(2), 308; https://doi.org/10.3390/biom16020308 - 14 Feb 2026
Viewed by 612
Abstract
Inflammatory bone loss is a shared pathological feature of chronic diseases such as periodontitis (PD) and rheumatoid arthritis (RA). Despite affecting distinct tissues, these diseases exhibit a bidirectional association and converge on common immune-mediated mechanisms of bone resorption. To uncover the molecular drivers [...] Read more.
Inflammatory bone loss is a shared pathological feature of chronic diseases such as periodontitis (PD) and rheumatoid arthritis (RA). Despite affecting distinct tissues, these diseases exhibit a bidirectional association and converge on common immune-mediated mechanisms of bone resorption. To uncover the molecular drivers underlying bone destruction across inflammatory comorbidities, we combined bioinformatic analyses with experimental validation, using PD and RA as clinically relevant models of inflammatory disease comorbidities. Elevated blood lactate levels were observed in murine models of PD and RA and correlated positively with disease severity. Single-cell RNA sequencing data from PD and RA cohorts revealed upregulation of lactate metabolism-related genes in specific monocyte subsets, accompanied by enhanced pro-inflammatory signaling and osteoclastogenic programs. Using multiple machine learning approaches, SAT1, TET2 and HIF1A were identified as core lactate-related genes with strong diagnostic potential for both diseases. In vivo and in vitro experiments further validated that lactate-driven reprogramming of monocytes, marked by activation of core lactate-related genes in circulating monocytes and local macrophages, functionally connects immune activation with exacerbated bone resorption in comorbid PD and RA. Together, these findings define a lactate-driven immunometabolic axis connecting immune responses and bone remodeling and identify SAT1, TET2 and HIF1A as potential biomarkers for inflammation-related bone loss. Full article
Show Figures

Figure 1

Back to TopTop