Home Research Feeds Salivary microbiota and inflammation-related proteins in patients with psoriasis

Salivary microbiota and inflammation-related proteins in patients with psoriasisOriginal paper

Researched by:

  • Karen Pendergrass

Last Updated: 2026-07-05

Karen Pendergrass
Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.

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Location
Denmark
Sample Site
Saliva
Species
Homo sapiens

What was studied?

This case-control study asked whether psoriasis alters the salivary microbiota and salivary inflammation-related proteins. It profiled saliva by 16S rRNA sequencing (V1-V3 region) and measured two proteins, NGAL and transferrin, by immunoassay. Data from psoriasis patients were compared to periodontitis patients and orally healthy controls. Linear discriminant effect size analysis identified differentiating bacterial taxa. Periodontal status was clinically examined to keep groups distinct.

Who was studied?

The study included 27 patients with psoriasis, 58 with periodontitis, and 52 orally healthy controls, recruited in Copenhagen, Denmark. Groups had comparable age and gender, with a mean age near 54 to 55 years. All participants were over 18 with at least 20 natural teeth. Psoriasis patients with treatment-requiring periodontitis were excluded, as were periodontitis patients with psoriasis. Stimulated saliva samples were collected and quality-controlled before sequencing.

What were the most important findings?

Salivary NGAL was significantly lower in psoriasis (996 ng/ml, standard error 320) than in periodontitis (2,072) or healthy controls (2,551), p less than 0.0001. Transferrin was also lowest in psoriasis (4.37 versus 7.25 and 10.02 ng/ml, p less than 0.0001). Linear discriminant analysis separated 52 taxa between psoriasis and periodontitis and 21 between psoriasis and controls. Periodontal pathogens such as Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Filifactor alocis were enriched in periodontitis. The core predominant genera and overall alpha-diversity did not differ across the three groups.

What are the greatest implications of this study?

The results suggest psoriasis leaves a measurable imprint on oral homeostasis, with a salivary microbiota and protein profile distinct from both periodontitis and health. Lower salivary NGAL and transferrin in psoriasis are notable and merit mechanistic study. This is described as the first characterization of the salivary microbiota in psoriasis. The modest psoriasis sample (n equals 27) and absence of blood and crevicular-fluid comparisons limit interpretation.

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