Mapping Mechanistic and Biological Evidence of Ganoderma lucidum-derived Bioactives in Periodontal Inflammation: A Scoping Review
DOI:
https://doi.org/10.24191/cos.v13i2.10133Keywords:
bioactives, host modulation, Ganoderma lucidum, periodontitis, periodontal inflammationAbstract
Objective: Periodontal inflammation is a host-mediated condition characterized by dysregulated immune and oxidative responses, prompting increasing interest in natural bioactives compounds with potential host-modulatory properties. Ganoderma lucidum has been widely studied for its anti-inflammatory and antioxidant activities; however, evidence relating specifically to periodontal inflammation remains limited and fragmented. This study aimed to conduct a scoping review of the available experimental literature on the biological and mechanistic roles of Ganoderma lucidum-derived bioactives in periodontal inflammation. Material and methods: Electronic searches were conducted in PubMed, Scopus, and Web of Science to identify English-language studies published between 2020 and 2025. Original preclinical experimental studies evaluating Ganoderma lucidum or its bioactives fractions in periodontal or gingival inflammation models were included. Data were descriptively summarized to outline the experimental models used, types of extracts, dosages applied, inflammatory and oxidative outcomes assessed, and the molecular pathways reported. Results: Four studies met the inclusion criteria. Three used in vivo rodent models, while one combined inflamed human gingival fibroblasts in vitro with a murine ligature-induced periodontitis model. Investigated preparations included polysaccharide extracts, ethanolic extracts, spore-oil fractions, and crude extracts. Across studies, administration was associated with reduced inflammatory mediators, including tumour necrosis factor-α, interleukin-1β, prostaglandin E2, matrix metalloproteinase-1, and interleukin-8, while one study reported increased interleukin-10. Some studies also reported reduced oxidative stress markers and lower alveolar bone loss. Mechanistic evidence was limited; one study suggested JNK-related signalling involvement, whereas NF-κB-related mechanisms were discussed more indirectly. Conclusions: The available evidence suggests that G. lucidum-derived preparations may be associated with anti-inflammatory, antioxidative, and tissue-protective effects in experimental models of periodontal inflammation. However, the evidence base remains limited, heterogeneous, and restricted to short-term preclinical studies. Further research incorporating standardized extract characterization, mechanistic validation, and human clinical evaluation is needed to clarify the translational relevance of these findings.
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