Evidence map›Paper›PMID 41750507›Full record

ReviewAntibiotics (Basel, Switzerland)2026

From Bench to Bedside: Personalized Genomics in the Diagnosis and Treatment of Osteomyelitis.

Amir Human Hoveidaei, Arian Rahimzadeh, Sara Mohammadi, Pranav Thota, Kimia Vakili, Parsa Yazdanpanahi, Ali Homaei, Seyed Arad Mosalamiaghili, Jakob Adolf, Janet D Conway

Abstract readReview
In one paragraph

Review in Antibiotics (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Amir Human HoveidaeiInternational Center for Limb Lengthening, Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore, Baltimore, MD 21215, USA.ORCID 0000-0003-4607-354X
Arian RahimzadehNeuromusculoskeletal Research Center, Iran University of Medical Sciences, Tehran 14535, Iran.ORCID 0009-0001-3732-4012
Sara MohammadiNeuromusculoskeletal Research Center, Iran University of Medical Sciences, Tehran 14535, Iran.ORCID 0009-0004-9281-4104
Pranav ThotaSchool of Medicine and Health Sciences, George Washington University, Washington, DC 20052, USA.
Kimia VakiliNeuromusculoskeletal Research Center, Iran University of Medical Sciences, Tehran 14535, Iran.ORCID 0000-0001-7296-3218
Parsa YazdanpanahiNeuromusculoskeletal Research Center, Iran University of Medical Sciences, Tehran 14535, Iran.ORCID 0009-0004-3969-2830
Ali HomaeiDepartment of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0001-5926-5482
Seyed Arad MosalamiaghiliNeuromusculoskeletal Research Center, Iran University of Medical Sciences, Tehran 14535, Iran.ORCID 0000-0002-3554-4935
Jakob AdolfDepartment of Paediatric Orthopaedics, Sofia Medical University, 1614 Sofia, Bulgaria.ORCID 0009-0006-0385-3940
Janet D ConwayInternational Center for Limb Lengthening, Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore, Baltimore, MD 21215, USA.ORCID 0000-0001-5694-3081

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteomyelitis (OM), an inflammatory condition of the bone tissue, is a complex orthopedic condition marked by chronic inflammation, diagnostic uncertainty, and recurrent infections. Despite standard treatments-including surgical debridement, antimicrobial therapy, and bone reconstruction-many patients continue to experience recurrence and treatment failure. Growing molecular evidence indicates that host genetic factors play a crucial role in shaping immune responses and influencing disease progression in OM. This narrative review synthesizes current knowledge from candidate gene single-nucleotide polymorphism (SNP) association studies to illustrate how specific genetic variations contribute to OM pathogenesis, diagnostic refinement, and treatment outcomes. We examined key immunogenetic variants within genes involved in inflammatory signaling, pathogen recognition, and neutrophil regulation. Our synthesis identifies a landscape of pro-inflammatory SNPs, such as IL-1β rs16944 and NLRP3 rs10754558, that are associated with increased susceptibility to chronic or post-traumatic OM, as well as SNPs that are associated with protective effects that may favor infection resolution, such as within the NOS2 and VDR genes. These SNP-driven differences in inflammasome activity, cytokine pathways, and oxidative stress responses highlight emerging opportunities for individualized therapeutic strategies. This review consolidates these variants, providing a genetic framework to analyze host susceptibility and differentiating high risk from protective genetic profiles. Integrating genomic insights into OM management represents a promising shift toward personalized medicine, enhancing diagnostic precision, informing targeted interventions, and improving prognostic assessment. Continued large-scale validation of candidate SNPs and translational genomic models will be essential to support their future clinical application.

Indexed as

host geneticsinterleukin-1βNLRP3 inflammasomeosteomyelitispersonalized medicinesingle nucleotide polymorphism

Identifiers

PMID41750507
PMCPMC12937331

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.