Gangani Dharmarathne

Dr. Gangani Dharmarathne


Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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6 November 2024 in Microorganisms
Verified
Journal Article
Open access
PDF file
GDGangani Dharmarathne
Gangani Dharmarathne
SKSamia Kazi
Samia Kazi
SKShalinie King
Shalinie King
TJThilini Nilusha Jayasinghe
Thilini Nilusha Jayasinghe
Cardiovascular diseases (CVDs) are a leading cause of widespread morbidity and mortality. It has been found that the gut and oral microbiomes differ in individuals with CVDs compared to healthy individuals. Patients with CVDs often require long-term pharmacological interventions. While these medications have been extensively studied for their cardiovascular benefits, emerging research indicates that they may also impact the diversity and composition of the oral and gut microbiomes. However, our understanding of how these factors influence the compositions of the oral and gut microbiomes in individuals remains limited. Studies have shown that statins and beta-blockers, in particular, cause gut and oral microbial dysbiosis, impacting the metabolism and absorption of these medications. These alterations can lead to variations in drug responses, highlighting the need for personalized treatment approaches. The microbiome’s role in drug metabolism and the impact of CVD medications on the microbiome are crucial in understanding these variations. However, there are very few studies in this area, and not all medications have been studied, emphasizing the necessity for further research to conclusively establish cause-and-effect relationships and determine the clinical significance of these interactions. This review will provide evidence of how the oral and gut microbiomes in patients with cardiovascular diseases (CVDs) interact with specific drugs used in CVD treatment.

26 March 2025 in Nutrients
Verified
Journal Article
Open access
PDF file
TJThilini Jayasinghe
Thilini Jayasinghe
JJJosie Jenkins
Josie Jenkins
NMNidhi Medara
Nidhi Medara
PCPhannaphat Choowong
Phannaphat Choowong
GDGangani Dharmarathne
Gangani Dharmarathne
ASAxel Spahr
Axel Spahr
Background: Dietary fibre plays a crucial role in metabolic regulation, inflammation, and microbiome composition. However, its impact on systemic and oral health, particularly in periodontitis, remains unclear. This study investigated the effects of high- and low-fibre diets on body composition, glycaemic control, inflammation, microbiome, and metabolome in a murine model of experimental periodontitis. Methods: Thirty-six male C57BL/6 mice were randomised to a high-fibre (40% fibre) or low-fibre (5% fibre) diet for eight weeks. Body weight, fat mass, lean mass, fasting blood glucose, serum inflammatory markers, alveolar bone loss, and root length were assessed. Oral and faecal microbiome composition was analysed using 16S rRNA sequencing. Metabolomic and short-chain fatty acid (SCFA) profiling was conducted using liquid chromatography–mass spectrometry (LC-MS). Results: Mice on the high-fibre diet exhibited significantly lower body weight (p < 0.0001), fat mass (p = 0.0007), and lean mass (p < 0.0001) compared to the low-fibre group. Fasting blood glucose levels were significantly lower in the high-fibre group (p = 0.0013). TNF-α and IFN-γ levels were significantly elevated in the low-fibre group (p < 0.0001), suggesting a heightened pro-inflammatory state. While alveolar bone loss and root length did not differ significantly, microbiome analysis revealed distinct bacterial compositions (PERMANOVA, p < 0.05), with fibre-fermenting taxa enriched in high-fibre-fed mice. Metabolomic analysis identified 19 significantly altered metabolites, indicating dietary adaptations. Conclusions: A high-fibre diet improves glycaemic control, reduces systemic inflammation, and alters microbial and metabolic profiles in experimental periodontitis. These findings highlight dietary fibre’s role in modulating metabolic and inflammatory pathways relevant to periodontal and systemic diseases.