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Published on: January 21, 2020
Parasites in Periodontal Health and Disease: A Systematic Review and Meta-analysis
David Felipe Martin-Garcia1, Malik Sallam2, Gabriela Garcia3,4,5
1Universidad Pontificia Comillas, Madrid, Spain.
Background:
Periodontitis is an inflammatory disease triggered by the infection of the periodontal sulcus by microbes. Together with the abundant eubacterial microbiota, at least two parasites have often been identified: the amoeba Entamoeba gingivalis and the flagellate Trichomonas tenax. The role of these protists in the pathophysiology of periodontal disease remains to be deciphered. A high diversity in their measured prevalence, mainly due to methodological concerns, prevents further analysis of the aetiological link between these parasites and periodontitis.
Methods:
To determine E. gingivalis and T. tenax prevalence in periodontal pockets as compared to healthy sulci, we have conducted a systematic review, searching 3 remote databases (Pubmed, LILACS, and Google Scholar), restricting to papers in which the diagnostic of the parasite was made using molecular methods. A total of 5 studies for E. gingivalis and 2 studies for T. tenax were included for the meta-analysis.
Results:
In the periodontal pockets, the prevalence of parasites is 76.9% (95%-CI: 71.5-81.7%) for E. gingivalis and 38.6% (95%-CI: 27.2-50.0%) for T. tenax . Both parasites are more abundant in periodontal pockets as compared to healthy sulci, with a risk ratio of 3.96 (95%-CI: 1.57-9.98) for E. gingivalis and 21.82 (95%-CI: 6.71-70.96) for T. tenax . The two subtypes of E. gingivalis exhibited the same risk ratio: 3.30 (95%-CI: 1.27-8.55) for ST1 and 3.30 (95%-CI: 0.42-26.03) for ST2, but ST1 was more prevalent (70.6%, 95%-CI: 65.0-76.2%) than ST2 (43.9%, 95%-CI: 35.5-52.4%) in periodontal pockets.
Conclusion:
Altogether, the data show that parasites are more prevalent in the diseased than in the healthy. However, the differences in prevalence between species and subtypes call for more studies to be able to conclude about their individual contributions in the pathophysiology of periodontal diseases. The heterogeneity in prevalence estimation should be investigated further, in particular to make out biological from methodological heterogeneity.
