Remission of Endometriosis by Hyperbaric Oxygen Treatment in Rats Original paper

What Was Studied?

This study, conducted by Aydin et al., investigated the effects of long-term hyperbaric oxygen therapy (HBOT) on experimentally induced endometriosis in a rat model. The primary objective was to assess whether HBOT could lead to remission of endometriotic lesions and alleviate inflammation by modulating peritoneal cytokine levels, particularly tumor necrosis factor-alpha (TNF-α). The study evaluated the volume, histopathological changes, and proliferation markers (Ki-67) of endometriotic implants after six weeks of HBOT.

Who Was Studied?

The study was performed on 40 non-pregnant, female Wistar-Albino rats. After surgical induction of endometriosis using an autotransplantation technique, the rats were divided into two groups: one receiving HBOT (20 rats) and a control group (19 rats) without treatment. HBOT was administered for 2 hours daily at 2.5 atm for six weeks. Both groups underwent multiple laparotomies to evaluate lesion volume, histopathological scores, and cytokine levels before and after treatment.

What Were the Most Important Findings?

The study demonstrated that HBOT resulted in complete remission of endometriotic lesions in a rat model. Significant reductions were observed in lesion volume, histopathological scores, Ki-67 proliferation markers, and TNF-α levels in the peritoneal fluid of the HBOT-treated group compared to controls. Specifically, the mean lesion volume decreased by 29.5% (57.4 ± 12.5 mm³ in the HBOT group vs. 94.6 ± 17.2 mm³ in controls). TNF-α levels were significantly lower in the HBOT group (5.33 ± 1.02 pg/mL vs. 8.16 ± 1.76 pg/mL in controls). Reduced Ki-67 staining indicated diminished cellular proliferation within endometriotic lesions. The findings suggest that HBOT alleviates endometriosis-associated inflammation by suppressing NFκB-mediated pro-inflammatory pathways and reducing TNF-α levels, key drivers of inflammation and angiogenesis in endometriosis.

From a microbiome perspective, while the study did not directly assess microbial changes, the reduction in hypoxia and inflammation could indirectly modulate microbial communities. Hypoxia-driven dysbiosis, favoring facultative anaerobes like E. coli and GBS, is a known contributor to endometriosis pathogenesis. By restoring oxygen levels and dampening inflammation, HBOT may reduce the selective advantage for these pathogens, potentially rebalancing the peritoneal microbiome.

What Are the Greatest Implications of This Study?

The study positions HBOT as a potential non-invasive therapeutic strategy for endometriosis, with demonstrated efficacy in reducing lesion size and inflammation. By targeting hypoxia and pro-inflammatory cytokines, HBOT addresses two critical drivers of endometriosis pathophysiology. This has implications for both clinical management and microbiome research, suggesting that HBOT could indirectly modulate microbial dysbiosis in endometriosis. However, the absence of direct microbial analyses leaves a critical gap in validating HBOT as a microbiome-targeted intervention (MBTI). Further studies incorporating microbiome sequencing and metabolomics are essential to establish a direct link between HBOT and microbiome modulation.