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Fluoroquinolone-Mediated Tendinopathy and Tendon Rupture
Ezgi Duman1, Sigrid Müller-Deubert1, Girish Pattappa1
1Department of Musculoskeletal Tissue Regeneration, Orthopaedic Hospital König-Ludwig-Haus, University of Würzburg, 97070 Würzburg, Germany.
Abstract:
The fluoroquinolone (FQ) class of antibiotics includes the world's most prescribed antibiotics such as ciprofloxacin, levofloxacin, and ofloxacin that are known for their low bacterial resistance. This is despite their potential to trigger severe side effects, such as myopathy, hearing loss, tendinopathy, and tendon rupture. Thus, healthcare organizations around the world have recommended limiting the prescription of FQs. Tendinopathy is a common name for maladies that cause pain and degeneration in the tendon tissue, which can result in tendon rupture. Whilst there are several identified effects of FQ on tendons, the exact molecular mechanisms behind FQ-mediated tendon rupture are unclear. Previous research studies indicated that FQ-mediated tendinopathy and tendon rupture can be induced by changes in gene expression, metabolism, and function of tendon resident cells, thus leading to alterations in the extracellular matrix. Hence, this review begins with an update on FQs, their mode of action, and their known side effects, as well as summary information on tendon tissue structure and cellular content. Next, how FQs affect the tendon tissue and trigger tendinopathy and tendon rupture is explored in detail. Lastly, possible preventative measures and promising areas for future research are also discussed. Specifically, follow-up studies should focus on understanding the FQ-mediated tendon changes in a more complex manner and integrating in vitro with in vivo models. With respect to in vitro systems, the field should move towards three-dimensional models that reflect the cellular diversity found in the tissue.
Insights
Fluoroquinolone (FQ) antibiotics can cause severe tendon issues. This review details how FQs damage tendon cells and extracellular matrix, leading to rupture, and suggests future research directions.
Area of Science:
- Pharmacology
- Biomedical Engineering
- Molecular Biology
Background:
- Fluoroquinolones (FQs) are widely prescribed antibiotics with low resistance but significant side effects.
- Tendon injuries, including tendinopathy and rupture, are serious adverse effects linked to FQ use.
- The precise molecular mechanisms underlying FQ-induced tendon damage remain incompletely understood.
Purpose of the Study:
- To review the current understanding of fluoroquinolone antibiotics, their mechanisms, and side effects.
- To explore the detailed effects of FQs on tendon tissue structure, cellular function, and the extracellular matrix.
- To discuss potential preventative strategies and future research avenues for FQ-mediated tendinopathy.
Main Methods:
- Review of existing literature on fluoroquinolones and tendon biology.
- Analysis of molecular and cellular changes induced by FQs in tendon tissue.
- Discussion of in vitro and in vivo models for studying FQ effects on tendons.
Main Results:
- FQ-mediated tendinopathy and rupture are associated with altered gene expression, metabolism, and function of tendon resident cells.
- These cellular changes lead to significant alterations in the extracellular matrix composition and integrity.
- Current understanding of FQ-induced tendon damage is limited, necessitating further investigation.
Conclusions:
- FQ antibiotics pose a risk of severe tendon damage, including rupture, through complex molecular pathways.
- Future research should integrate in vitro and in vivo models, emphasizing advanced 3D in vitro systems to mimic in vivo complexity.
- A deeper understanding is crucial for developing preventative measures against FQ-induced tendinopathy.
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