Entamoeba gingivalis: The Gum Amoeba

Entamoeba gingivalis is a single-celled amoeba that lives in the human mouth, above all in the pockets that open between teeth and inflamed gums. Described from dental plaque in 1849, it was the first amoeba found in a human being. In 1914 doctors blamed it for gum disease, but after a controversy that idea was almost entirely abandoned [1]. Studies using genetic tests now find it about four times as often in diseased gum pockets as in healthy gum crevices [2], and laboratory experiments show that it can eat living gum cells and set off strong inflammation [3][4]. Whether it helps cause gum disease, or simply thrives in it, is still an open question [1].

Table of Contents

  1. What Entamoeba gingivalis Is
  2. Where It Lives
  3. How Common It Is
  4. The Link With Gum Disease
  5. How It Damages Gum Tissue
  6. History: From “Amoebic Pyorrhea” to Rediscovery
  7. How It Is Detected
  8. Treatment Research
  9. Ivermectin and the Gum Amoeba
  10. Key Research Papers
  11. Connections
  12. Featured Videos

What Entamoeba gingivalis Is

The gum amoeba is a protozoan: a single-celled organism, larger and more complex than a bacterium. It is a close relative of Entamoeba histolytica, the cause of amoebiasis [1], which inflames and destroys tissue in the colon [3]. The mouth holds a second single-celled parasite, the flagellate Trichomonas tenax, which swims with whip-like tails, and the two are often studied together [5].

The form seen under the microscope is the trophozoite (the active, feeding form). A 2018 review describes it as about 30 micrometers across (a micrometer is a thousandth of a millimeter). It moves by pushing out pseudopods, temporary extensions of the cell, and it swallows bacteria and human cells [1]. It is anaerobic, living without oxygen [6], and it is found mainly in gum pockets, which suggests that low oxygen matters for its survival [1].

Long thought to have no cyst stage

Most Entamoeba species also form cysts: resting forms with a protective wall that survive in the environment and carry the infection to new hosts [1]. The gum amoeba was long thought to be the exception. A 1989 study described it as having no resistant forms (cysts) [7]. The 2018 review notes that cysts were reported in the early 1900s, yet it became “commonly accepted” that the gum amoeba does not produce them, taking the absence of proof as proof of absence [1]. In 2023, a laboratory study found that it can form cyst-like structures with walls of chitin (the tough material of insect shells) when exposed to antibiotics, as described under Treatment Research [6].

A virus that lives inside it

Redondoviruses are DNA viruses found in many healthy people and more abundant in mouth and airway samples from people with periodontitis, acute illness or severe coronavirus disease 2019 (COVID-19). A 2023 study identified the gum amoeba as their likely host: the two occurred together in genetic data, and amoebae grown in the laboratory were strongly positive for the virus. The authors, who call the amoeba a commensal (an organism that lives on its host without harming it), concluded that bacteria are not the only residents of the human body that host abundant human-associated viruses [8].

Where It Lives

A 2021 worldwide review lists dental plaque, the surfaces of the gums and teeth, the spaces between teeth and areas of tooth decay as places where the gum amoeba is found [9]. Its main home is the periodontal pocket. Around a healthy tooth the gum forms a shallow groove less than 3 millimeters deep. In periodontitis the gum’s attachment to the tooth breaks down, the groove deepens into a pocket, plaque gathers in it and oxygen is scarce [1]. The amoeba also lives in healthy mouths: in the 2020 and 2021 studies described below, 15% of healthy mouths carried it, and it can be present without symptoms [3][4].

In dogs and cats

The 2018 review notes that the amoeba is often seen in the gum pockets of pets as well as people [1]. A 2026 study in Guangxi, China, tested 93 people, 298 dogs and 325 cats, and found the gum amoeba in more than 90% of all three, mostly as mixed infections of two subtypes (described below). Its genetic sequences grouped together regardless of host species, which the authors took as a sign that it can pass between species. They concluded that it “likely acts as a commensal” [10].

A 2022 case report described a 13-year-old dog with three months of sneezing, nosebleeds from both nostrils and nasal discharge, along with severe gum disease. Fluid flushed from its nose contained amoebae, which genetic testing identified as the gum amoeba. The dog improved dramatically on the antibiotic clindamycin and was clinically normal four weeks after a dental cleaning with several extractions [11].

Outside the mouth

How it spreads

How the gum amoeba passes from one host to another is not settled. The 2018 review notes that without a cyst it would have to travel as a trophozoite able to withstand oxygen, and that its full life cycle has not been described [1]. The 2023 cyst study’s authors wrote that cyst formation has “significant implications for dissemination and infection” [6], and the 2026 study of people and pets points to spread between species [10].

How Common It Is

A 2021 review pooled 52 studies with 7,596 participants and estimated the gum amoeba’s worldwide prevalence at 37%. Rates ranged from 87% in Jordan to 3% in Portugal. By World Health Organization region the Americas had the highest pooled rate (56%), and by age, groups with a mean age of 46 to 55 (61%) [9].

Studies around the world

In people with weakened immune defenses

A 2013 study found the gum amoeba in 63.4% (52 of 82) of people with human immunodeficiency virus (HIV) infection or acquired immunodeficiency syndrome (AIDS). Its presence was not linked to their CD4 immune-cell counts or virus levels, and it did not behave as an opportunistic infection (one that takes advantage of weakened immunity), which the authors suggested may relate to the HIV treatment all of them were taking [18]. A 1994 study found the amoeba more often in people receiving chemotherapy than in healthy controls [19].

Subtypes: ST1, ST2 “kamaktli” and ST3

In 2018, researchers described an amoeba sharing the gum amoeba’s niche whose ribosomal genetic sequence was 89% identical to it. They named it the “kamaktli variant” and proposed it as subtype 2 (ST2), alongside the original subtype 1 (ST1) [20]. The same team found both subtypes in all three groups they tested, and suggested that the two may be separate species [21]:

A 2022 review found the same risk ratio for diseased pockets with both subtypes (3.30 each, though the figure for ST2 was uncertain), and found ST1 more common in pockets (70.6%) than ST2 (43.9%) [2]. In the Tehran study, 75% of positive samples were ST1 and 25% ST2 [16]. In a 2019 study of 50 samples from people with periodontitis, 50% carried ST1, and 12 of the remaining 25 carried ST2 [22]. A 2023 study in Austria found a possible third subtype, ST3, only alongside ST1 [14].

Gum disease develops in stages: dental plaque builds up, gingivitis (inflammation of the gums caused by the plaque) follows, and in periodontitis the bone and fibers that hold the teeth in place are permanently damaged. Periodontitis affects about half of the world’s adults and eventually leads to tooth loss. The accepted models explain it through changes in the bacteria of the gum crevices. The 2018 review argued that the possible role of protozoa “has been ignored” and proposed that the gum amoeba be reassessed as a potential contributor [1].

The 2020 Journal of Dental Research study

A 2020 study began with a genetic survey of inflamed gum pockets, in which the gum amoeba’s ribosomal RNA was the second most abundant after human RNA. Stained gum tissue from people with severe chronic periodontitis showed the amoeba among large numbers of neutrophils (white blood cells that attack microbes). The researchers then tested 158 people with periodontitis and healthy controls by microscopy and by polymerase chain reaction (PCR), a test that copies and detects a stretch of the amoeba’s DNA. In the people with periodontitis, they found it in 77% of inflamed gum sites and 22% of healthy sites, and 15% of healthy mouths carried it. The authors called the gum amoeba “a potential and, to date, underrated microbial driver of destructive forms of periodontitis” [3].

Pooled analyses

The Jordan PCR study

A 2021 study in Jordan tested saliva and dental plaque from 237 people by PCR. The gum amoeba was present in 88.9% of people with periodontitis, 84.9% of those with gingivitis and 47.9% of healthy people. Carriers had 6.6 times the odds of gum disease (6.1 for gingivitis, 6.4 for periodontitis). Gum disease was also linked to lower income, lack of dental care and diabetes. The authors concluded that “the dogmatic view” of the mouth parasites as harmless commensals “needs to be re-evaluated” [24].

More studies in people

Around dental implants

Peri-implantitis is inflammation with bone loss around a dental implant. A 2020 study of 141 people found no parasites around 40 healthy implants, but found the gum amoeba in 31 of 101 peri-implantitis lesions (30.7%), more often in the lower jaw than the upper [27]. A 2026 study of 140 people found both mouth parasites more often around diseased implants than healthy ones, at similar rates on teeth and implants in the same mouth, and linked their presence to periodontitis and its severity independently of other factors [28].

What the association does and does not show

The 2026 implant study’s authors cautioned that protozoa found at diseased sites “may not imply a direct causal relationship with the disease” [28]. The 2018 review notes that without a reliable animal model of infection, the amoeba’s role cannot be settled by Koch’s postulates, the classic criteria for proving that a single germ causes a disease, and that research is needed to determine whether it takes part in the disease or is just a marker of it [1]. A 2023 study pointed out that the amoeba is also regularly found in healthy people, so its precise role “remains to be established” [14]. A 2023 review, on the other hand, concluded that both mouth parasites “may cause periodontal disease” [5].

How It Damages Gum Tissue

Much of the evidence on how the gum amoeba harms tissue comes from laboratory experiments with gum cells, and from its resemblance to Entamoeba histolytica, which kills and eats human cells [1].

Invasion where the surface is broken

The 2020 study showed that once the gum’s protective surface layer (the epithelium) was disrupted, the gum amoeba invaded the gum tissue, moved through it and fed on the body’s cells. The authors concluded that its ways of invading and destroying tissue are similar to those of Entamoeba histolytica in the colon [3]. A 2021 follow-up describes it as able to invade torn lining of the mouth, where it eats fragments of live cells [4]. A 1994 study, by contrast, found no amoebae invading the tissue in gum sections from people with periodontitis [19]. The 2020 authors also point to the known resistance of Entamoeba species to neutrophils, to antimicrobial peptides (germ-killing molecules made by the body) and to various antibiotics [3].

Eating living cells

The 2018 review shows video-microscope frames of an amoeba in a gum pocket drawing in material from what was probably a white blood cell, and notes that it can engulf one or more human cells at a time. Neutrophils, the white blood cells that predominate in gum pockets, may be its main target, and the review argues that this leaves the body’s first line of cellular defense in the pocket unable to do its job [1]. In 2021, laboratory experiments showed the amoeba killing live gum surface cells by trogocytosis: nibbling off and swallowing pieces of a living cell [4].

Inflammation signals

In gum surface cells grown in the laboratory, the 2020 study found that the amoeba raised interleukin 8, an inflammation signal that draws neutrophils into tissue [1], about 1,900-fold. The mouth pathogen Porphyromonas gingivalis did not do this in the same test. In gum connective-tissue cells (fibroblasts) the amoeba raised the collagen-cutting enzyme matrix metalloproteinase 13 by 11-fold, and direct contact with it held back the multiplication of gum surface cells [3]. In the 2021 study, which read the activity of the genes in infected gum cells, the most strongly raised genes in surface cells were the inflammation signals tumor necrosis factor (430-fold) and interleukin 8 (359-fold), while fibroblasts showed changes in cell-cycle and growth-arrest genes [4]. A 2023 review concluded that both mouth parasites can drive inflammation in gum tissue by raising inflammatory molecules and recruiting neutrophils [5].

History: From “Amoebic Pyorrhea” to Rediscovery

The gum amoeba was first described in 1849, from dental plaque, as “Amoebea gengivalis”: the first amoeba found in humans. Doubts about whether it causes disease were raised as early as 1893 [1].

1914: “amoebic pyorrhea” and emetine

Gum disease was then called pyorrhea alveolaris. In 1914, a study of patients at the Philadelphia Hospital found amoebae in all 46 people with pyorrhea it examined, and the researchers later reported finding none in 7 healthy people from the same group. Patients were given emetine, an alkaloid (a plant compound) then thought to kill amoebae while having little effect on bacteria. According to the 1914 report, the amoebae disappeared and the pyorrhea was cured in 13 patients. The researchers concluded that the amoeba caused the disease and renamed it “amoebic pyorrhea” and “oral endamebiasis” [1]. The full story is on the page Amoebic Pyorrhea and Emetine.

Controversy and abandonment

The 2018 review describes how these studies, some with few participants, “were countered by specialist opinions without formal experimental proofs”, as reported in 1916, and how “this controversy led to an almost total abandon of the etiology- and emetine-based therapy”. Critics in 1925 said the cure did not last, citing relapses; the review describes these claims as unsupported by data and as ignoring the possibility of re-infection. A 1925 laboratory test found that emetine had “no very marked amoebicidal action” on cultured gum amoebae, but the review judges the test’s method inaccurate [1].

Decades of microscope studies

Only a few microscope studies followed, but almost all of them, from 1927 to 1989, found the amoeba in close to 100% of advanced periodontal pockets. In healthy gum crevices, where these studies looked, rates ranged from 0 to 26%, which the review suggests may reflect errors in identifying the amoeba [1]. A 1989 study, noting that medical interest faded once the amoeba was also found in healthy people, found it in 18 of 78 patients with gum disease (23.07%) and in none of 117 dental students or 57 patients with other mouth conditions [7].

The genetic era

In 1995 a gene of the gum amoeba was sequenced, opening the way to identifying it with PCR. The first PCR study, in 1996, used a method the review calls sub-optimal and found the amoeba in 2 of 32 diseased sites (6.25%) and none of 20 healthy sites. A 2011 study using real-time PCR found it in 69.2% of periodontitis sites and none of 12 healthy sites. A 2017 study of genetic activity in gum samples found it in all 4 periodontal pockets examined, with less of it, or none, in healthy sites [1].

How It Is Detected

Samples are taken from the gum pocket or the plaque around the teeth, with a curette (a small scraping instrument), a probe or absorbent paper, and some studies also test saliva [27][24]. Three kinds of test are used.

Microscopy

The oldest method is looking for the moving amoeba in a fresh, wet sample under the microscope, or in a smear stained with a dye, as in a 1989 study [7]. The 2018 review suggests that some older microscope studies may have misidentified the amoeba [1], while the 2014 study confirmed by PCR that the amoebae seen under the microscope in gum pockets were mainly, if not exclusively, the gum amoeba [25].

Culture

Culture means growing the amoeba in the laboratory, where it is kept with bacteria as food [8]. The 2018 review calls culture “a bottleneck” for research on the gum amoeba [1]. In the 2020 study of 315 adolescents, culture detected it in 9.2% and PCR in 11.4% [15]. A 2023 review judged culture and molecular (DNA-based) tests the best tools for detecting both mouth parasites [5].

Polymerase chain reaction

PCR detects the amoeba’s DNA and can tell its subtypes apart. The 2014 study designed a new set of primers (short pieces of DNA that pick out the stretch to be copied) specific to the gum amoeba, and reported strong sensitivity for PCR compared with clinical diagnosis (58 of 72 samples, 81%) and with microscopy (51 of 65, 78%) [25]. In 2019, researchers developed a real-time PCR (a version that measures the DNA as it is copied) that detects both subtypes and measures the parasite load. They proposed using it before and after gum treatment to follow the treatment’s effect [22]. Other studies use nested PCR (two rounds of copying) followed by DNA sequencing to identify subtypes [16], or sequence the DNA of all the microbes in plaque and use fluorescent probes to show where the amoeba sits [26]. Across 52 studies, molecular tests found the amoeba more often than direct examination (53% versus 36%) [9].

Treatment Research

Standard care for periodontitis, the 2018 review notes, is based on mechanical and/or surgical removal of dental plaque, tartar and damaged or inflamed tissue. In the review authors’ view, this deals with late symptoms without addressing the possible causes [1].

Metronidazole

Metronidazole is a drug used to treat infections caused by protozoa [29]. A 1989 study began after the gum amoeba was found in the gum fluid of a 19-year-old man with chronic gum disease who was cured after metronidazole treatment [7]. In a 1994 study, metronidazole treatment of people with periodontitis reduced how often the amoeba was found [19]. In the 2020 study of adolescents, those with a history of antibiotic use were significantly less likely to carry it [15].

Antibiotics and cyst-like forms

A 2023 laboratory study grew strains of the amoeba taken from inflamed gum pockets for 8 days, with or without the antimicrobial drugs amoxicillin and metronidazole. With the drugs, the amoebae formed cyst-like structures: smaller than the free-living form, with smooth surfaces, angular edges and walls containing chitin, as in the cysts of other Entamoeba species. The authors concluded that cyst formation “may explain why established treatment approaches often fail to halt periodontal tissue destruction during periodontitis and peri-implantitis” [6].

Mouth rinses in the laboratory

A 2019 laboratory study tested reference strains of the gum amoeba and Trichomonas tenax against metronidazole and 14 mouth-rinse agents: 20% benzocaine (a local anesthetic), 0.2% chlorhexidine (an antiseptic) and 12 commercially sold rinses, among them a sage tincture. Used undiluted, every rinse killed both protozoa. Chlorhexidine was highly effective, and the authors wrote that benzocaine has properties that could support anti-protozoal treatment [29]. The tests were on amoebae in laboratory culture, not in people’s gum pockets.

Ivermectin and the Gum Amoeba

Ivermectin is an antiparasitic medicine. In online chat groups, people describe applying ivermectin paste directly to their gums, on the theory that parasites living in the gum tissue drive gum disease. The idea has a precedent in the 1914 reports, in which an anti-amoeba drug, emetine, was said to clear the amoeba and cure the gum disease [1]. The chat accounts, and published case reports of ivermectin used against other parasites in the tissues of the mouth, are collected on the page Ivermectin for Gum Disease.

None of the studies of the gum amoeba gathered for this page tested ivermectin against it, in the laboratory, in animals or in people, so they say nothing either way about whether ivermectin affects this amoeba. The substances tested or used against it in these studies are emetine, metronidazole, amoxicillin with metronidazole, mouth rinses and clindamycin, all described in the sections above.

Key Research Papers

  1. Bonner M, Fresno M, Gironès N, Guillén N, Santi-Rocca J. Reassessing the Role of Entamoeba gingivalis in Periodontitis. Front Cell Infect Microbiol. 2018;8:379. PubMed PMID: 30420943
  2. Martin-Garcia DF, Sallam M, Garcia G, Santi-Rocca J. Parasites in Periodontal Health and Disease: A Systematic Review and Meta-analysis. Adv Exp Med Biol. 2022;1373:95-111. PubMed PMID: 35612794
  3. Bao X, Wiehe R, Dommisch H, Schaefer AS. Entamoeba gingivalis Causes Oral Inflammation and Tissue Destruction. J Dent Res. 2020;99(5):561-567. PubMed PMID: 32023135
  4. Bao X, Weiner J, Meckes O, Dommisch H, Schaefer AS. Entamoeba gingivalis Exerts Severe Pathogenic Effects on the Oral Mucosa. J Dent Res. 2021;100(7):771-776. PubMed PMID: 33792418
  5. Santos JO, Roldán WH. Entamoeba gingivalis and Trichomonas tenax: Protozoa parasites living in the mouth. Arch Oral Biol. 2023;147:105631. PubMed PMID: 36764082
  6. Becker C, Adam A, Dommisch H, Stach T, Schaefer AS. In vitro induction of Entamoeba gingivalis cyst-like structures from trophozoites in response to antibiotic treatment. Front Cell Infect Microbiol. 2023;13:1201394. PubMed PMID: 37469604
  7. Sefer M, Boanchis AI, Chaouki SH, Ganescu V, Constantin P. [Periodontal diseases with Entamoeba gingivalis]. Rev Chir Oncol Radiol O R L Oftalmol Stomatol Ser Stomatol. 1989;36(4):279-85. PubMed PMID: 2535047
  8. Keeler EL, Merenstein C, Reddy S, Taylor LJ, Cobián-Güemes AG, Zankharia U, et al. Widespread, human-associated redondoviruses infect the commensal protozoan Entamoeba gingivalis. Cell Host Microbe. 2023;31(1):58-68.e5. PubMed PMID: 36459997
  9. Badri M, Olfatifar M, Abdoli A, Houshmand E, Zarabadipour M, Abadi PA, et al. Current Global Status and the Epidemiology of Entamoeba gingivalis in Humans: A Systematic Review and Meta-analysis. Acta Parasitol. 2021;66(4):1102-1113. PubMed PMID: 34050504
  10. Luo B, Yin Z, Liang S, She X, Otranto D, Fang F. High prevalence and cross-species transmission potential of Entamoeba gingivalis and Trichomonas tenax in humans, dogs, and cats in Guangxi, China. Acta Trop. 2026;280:108198. PubMed PMID: 42323966
  11. Randolph NK, McAloney CA, Ossiboff R, Hernandez B, Cook M, Hokamp JA. Nasal colonization by Entamoeba gingivalis in a 13-year-old Italian Greyhound. Vet Clin Pathol. 2022;51(2):269-272. PubMed PMID: 35274349
  12. Dao AH. Entamoeba gingivalis in sputum smears. Acta Cytol. 1985;29(4):632-3. PubMed PMID: 3861055
  13. Bradbury RS, Roy S, Ali IK, Morrison JR, Waldner D, Hebbeln K, et al. Case Report: Cervicovaginal Co-Colonization with Entamoeba gingivalis and Entamoeba polecki in Association with an Intrauterine Device. Am J Trop Med Hyg. 2019;100(2):311-313. PubMed PMID: 30526733
  14. Köhsler M, Kniha E, Wagner A, Walochnik J. Pilot Study on the Prevalence of Entamoeba gingivalis in Austria-Detection of a New Genetic Variant. Microorganisms. 2023;11(5). PubMed PMID: 37317068
  15. Sharifi M, Jahanimoghadam F, Babaei Z, Mohammadi MA, Sharifi F, Hatami N, et al. Prevalence and Associated-Factors for Entamoeba gingivalis in Adolescents in Southeastern Iran by Culture and PCR, 2017. Iran J Public Health. 2020;49(2):351-359. PubMed PMID: 32461943
  16. Tahmasebi E, Ghanimatdan M, Hajisadeghi S, Rafiei E, Sharifi Y, Jafari Nodoushan Z, et al. A Case Control Study to Assess Frequency, Risk Factors and Genetic Diversity of Entamoeba gingivalis. Oral Dis. 2025;31(10):2954-2963. PubMed PMID: 40420465
  17. Oladokun AO, Ogboru P, Opeodu OI, Lawal AO, Falade MO. Prevalence of Entamoeba gingivalis and Trichomonas tenax among patients with periodontal disease attending Dental Clinic, University College Hospital, Ibadan. Trop Parasitol. 2023;13(2):107-113. PubMed PMID: 37860615
  18. Cembranelli SB, Souto FO, Ferreira-Paim K, Richinho TT, Nunes PL, Nascentes GA, et al. First evidence of genetic intraspecific variability and occurrence of Entamoeba gingivalis in HIV(+)/AIDS. PLoS One. 2013;8(12):e82864. PubMed PMID: 24376598
  19. el Azzouni MZ, el Badry AM. Frequency of Entamoeba gingivalis among periodontal and patients under chemotherapy. J Egypt Soc Parasitol. 1994;24(3):649-55. PubMed PMID: 7844431
  20. García G, Ramos F, Martínez-Hernández F, Hernández L, Yáñez J, Gaytán P. A new subtype of Entamoeba gingivalis: "E. gingivalis ST2, kamaktli variant". Parasitol Res. 2018;117(4):1277-1284. PubMed PMID: 29429011
  21. Garcia G, Ramos F, Maldonado J, Fernandez A, Yáñez J, Hernandez L, et al. Prevalence of two Entamoeba gingivalis ST1 and ST2-kamaktli subtypes in the human oral cavity under various conditions. Parasitol Res. 2018;117(9):2941-2948. PubMed PMID: 29987412
  22. Zaffino M, Dubar M, Debourgogne A, Bisson C, Machouart M. Development of a new TaqMan PCR assay for the detection of both Entamoeba gingivalis genotypes. Diagn Microbiol Infect Dis. 2019;95(4):114886. PubMed PMID: 31522801
  23. Moosazadeh M, Sabeti MA, Hashemi SM, Ghazalgoo A, Mousavi T, Mahdavi S, et al. THE RELATIONSHIP BETWEEN ENTAMOEBA GINGIVALIS AND TRICHOMONAS TENAX WITH PERIODONTITIS AND GINGIVITIS: A SYSTEMATIC REVIEW, META-ANALYSIS, AND META-REGRESSION. J Evid Based Dent Pract. 2025;25(3):102141. PubMed PMID: 40716826
  24. Yaseen A, Mahafzah A, Dababseh D, Taim D, Hamdan AA, Al-Fraihat E, et al. Oral Colonization by Entamoeba gingivalis and Trichomonas tenax: A PCR-Based Study in Health, Gingivitis, and Periodontitis. Front Cell Infect Microbiol. 2021;11:782805. PubMed PMID: 34950608
  25. Bonner M, Amard V, Bar-Pinatel C, Charpentier F, Chatard JM, Desmuyck Y, et al. Detection of the amoeba Entamoeba gingivalis in periodontal pockets. Parasite. 2014;21:30. PubMed PMID: 24983705
  26. Jiao J, Bie M, Xu X, Duan D, Li Y, Wu Y, et al. Entamoeba gingivalis is associated with periodontal conditions in Chinese young patients: A cross-sectional study. Front Cell Infect Microbiol. 2022;12:1020730. PubMed PMID: 36275028
  27. Arpağ OF, Kaya ÖM. Presence of Trichomonas tenax and Entamoeba gingivalis in peri-implantitis lesions. Quintessence Int. 2020;51(3):212-218. PubMed PMID: 32020131
  28. Sari A, Kaya OM, Arisan V, Nibali L. The association between Trichomonas tenax and Entamoeba gingivalis and periimplantitis and periodontitis. Clin Oral Investig. 2026;30(8). PubMed PMID: 42467269
  29. Moroz J, Kurnatowska AJ, Kurnatowski P. The in vitro activity of selected mouthrinses on the reference strains of Trichomonas tenax and Entamoeba gingivalis. Ann Parasitol. 2019;65(3):257-265. PubMed PMID: 31599542

PubMed Topic Searches

  1. PubMed: Entamoeba gingivalis and periodontitis
  2. PubMed: Entamoeba gingivalis prevalence by PCR
  3. PubMed: Entamoeba gingivalis subtypes
  4. PubMed: Entamoeba gingivalis and peri-implantitis
  5. PubMed: Entamoeba gingivalis treatment

Back to Table of Contents

Connections

Back to Table of Contents