Dunn · Arthritis & rheumatology (Hoboken, N.J.) 2020 · Case-control tissue study with animal model comparison · n=75

Identification of Cartilage Microbial DNA Signatures and Associations With Knee and Hip Osteoarthritis.

Cited 102 times in the scientific literature.

Level 4 - case-series / case-control

Case-control tissue analysis with animal model comparison

PubMed 31961065 · doi:10.1002/art.41210 · record verified 2026-08-29

What was done

Researchers characterized microbial DNA profiles in human and mouse articular cartilage. Using 16S ribosomal RNA gene deep sequencing, they analyzed eroded and intact cartilage from knee osteoarthritis patients (n = 21 eroded, 21 intact samples) and hip osteoarthritis patients (n = 34 eroded, 33 intact samples), compared to cadaver controls (n = 10 knee, 10 hip samples). Metagenomic profiles were reconstructed, confirmation was performed in an independent cohort by clade-specific quantitative PCR, and results were compared with cartilage from osteoarthritis-susceptible C57BL/6 and resistant MRL/MpJ mice, with germ-free mice as controls.

What was found

Microbial alpha diversity was significantly decreased in human osteoarthritis versus control samples (P < 0.0001) and in hip versus knee samples (P < 0.0001). Osteoarthritis cartilage microbial DNA showed increased gram-negative constituents (P = 0.02). Reconstructed functional analyses showed increases in lipopolysaccharide production (P = 9.9 x 10^-3), phosphatidylinositol signaling (P = 4.2 x 10^-4), and nitrogen metabolism (P = 8 x 10^-3), and decreases in sphingolipid metabolism (P = 7.7 x 10^-4). Similar clade differences occurred when comparing osteoarthritis-susceptible to resistant mice.

Why it matters

This study provides evidence of cartilage-specific microbial DNA signatures that shift toward gram-negative patterns in osteoarthritis, identifying potential host-microbe interactions in joint pathology.

Limits

The human sample size was modest (55 osteoarthritis patients and 20 cadaver controls). The cross-sectional design cannot determine whether microbial DNA changes cause joint degradation or result from increased vascularity/permeability in diseased tissue, and 16S rRNA sequencing identifies bacterial DNA fragments rather than viable bacteria.

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