Microbial changes in relation to oral mucositis in autologous hematopoietic stem cell transplantation recipientsOriginal paper
What was studied?
This study tracked how the oral microbiome changes over time in relation to ulcerative oral mucositis after autologous stem cell transplantation. It also tested whether specific bacteria before transplant could predict who develops mucositis, and how fungal load changes. Oral rinse samples were collected before transplant, three times weekly during hospitalization, and three months after. The microbiome was profiled by 16S ribosomal RNA amplicon sequencing and fungal load measured by quantitative PCR.
Who was studied?
The cohort was 51 multiple myeloma patients at two centers in the Netherlands, all treated with high-dose melphalan followed by autologous transplant. Mean age was 57.4 years; 28 were male and 23 female. This was a prospective human study. Patients were grouped by WHO oral mucositis score. Twenty (39%) developed ulcerative mucositis (WHO 2 or higher), while 31 had no or only mild non-ulcerative mucositis. In total 245 samples were analyzed.
What were the most important findings?
The oral microbiome shifted significantly after transplant (PERMANOVA P = 0.0001) and returned to baseline by three months. Changes were faster and more pronounced in mucositis patients, who showed reduced Shannon diversity and higher dominance already at week 1. Before transplant, 13 taxa discriminated the groups. Fungal DNA appeared in 91% of samples, and mucositis patients had a significantly higher fungal proportion at three months (P = 0.036). Mucositis patients also had longer hospital stays (24.5 vs 20.2 days, P = 0.005).
What are the greatest implications of this study?
The findings suggest that a more resilient oral microbiome, and distinct taxa present before transplant, mark patients less likely to develop ulcerative mucositis. This raises the possibility of microbially driven risk factors and prognostic biomarkers. The authors note that cause and consequence remain hard to separate, since a less severe disease phenotype could also explain the pattern. They call for larger studies to clarify the host-microbe interactions involved.