Bone and TNF in rheumatoid arthritis: clinical implications

Maria Manara1, Luigi Sinigaglia1

  • 1Department of Rheumatology , Gaetano Pini Institute , Milan , Italy.

RMD Open
|November 12, 2015
PubMed

Insights

Tumor necrosis factor (TNF) inhibitors help reduce bone loss and joint damage in rheumatoid arthritis (RA). However, evidence for their effectiveness in preventing fractures remains limited.

Area of Science:

  • Rheumatology
  • Immunology
  • Bone Metabolism

Background:

  • Tumor necrosis factor (TNF) is implicated in bone loss associated with rheumatoid arthritis (RA).
  • TNF inhibitors are used to manage RA, impacting systemic and local bone loss.

Purpose of the Study:

  • To evaluate the clinical effectiveness of TNF inhibitors in rheumatoid arthritis, focusing on bone loss and fracture prevention.
  • To compare the efficacy of TNF inhibitors against methotrexate in reducing radiographic progression in RA patients.

Main Methods:

  • Analysis of clinical trial data on TNF inhibitors in RA patients.
  • Review of observational studies assessing anti-TNF therapy outcomes.
  • Assessment of bone mineral density and bone turnover markers.
  • Evaluation of radiographic progression and joint damage evolution.

Main Results:

  • TNF inhibitors effectively arrested systemic bone loss, as indicated by bone mineral density and turnover markers.
  • Limited evidence exists for a clinically significant effect of TNF inhibition on fracture prevention.
  • Randomized clinical trials demonstrated higher efficacy of TNF inhibitors in reducing radiographic progression compared to methotrexate.
  • Observational studies support the effectiveness of anti-TNF therapy in mitigating joint damage progression.

Conclusions:

  • TNF inhibitors are effective in managing bone loss and radiographic progression in rheumatoid arthritis.
  • Further research is needed to establish the role of TNF inhibitors in fracture prevention in RA patients.

Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.3K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
749
Connective Tissue Cell Types01:22

Connective Tissue Cell Types

Connective tissue develops from the mesoderm of a developing embryo and consists of cells, fibers, and ground substance: a gel-like material containing large complexes of carbohydrates and proteins. Connective tissue was first identified as a separate tissue family in the 18th century, and Johannes Peter Muller coined the term connective tissue.
Fat cells (adipocytes), smooth muscle cells (myoblasts), and bone cells (osteoblasts) are some connective tissue cell types. Some immune system cells...
4.5K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
13.9K
Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies

The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
1.0K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
10.3K