Entamoeba gingivalis is a protozoan that resides in the oral cavity. Using molecular biology techniques, we identified a novel organism that. The protozoan Entamoeba gingivalis resides in the oral cavity and is frequently observed in the periodontal pockets of humans and pets. The amoeba Entamoeba gingivalis is the most common micro-organism found in all cases of periodontal diseases. It’s presence is easy to confirm by using a.
|Published (Last):||27 June 2006|
|PDF File Size:||19.52 Mb|
|ePub File Size:||17.43 Mb|
|Price:||Free* [*Free Regsitration Required]|
Recent Progresses in Amebiasis. The protozoan Entamoeba gingivalis resides in the oral cavity and is frequently observed in the periodontal pockets of humans and pets. This species of Entamoeba is closely related to the human pathogen Entamoeba histolyticathe agent of amoebiasis. Periodontitis entamoebx half the adult population in the world, eventually leads to edentulism, and has been linked to other pathologies, like diabetes and cardiovascular diseases. As aging is a risk factor for entwmoeba disorder, it is considered an inevitable physiological process, even though it can be prevented and cured.
However, the impact of periodontitis on the patient’s health and quality of life, as well as its economic burden, are underestimated.
Commonly accepted models explain the progression from health to gingivitis and then periodontitis by a gradual change in the identity and proportion of bacterial microorganisms in the gingival crevices.
Though not pathognomonic, inflammation is always present in periodontitis. The recruitment of leukocytes to inflamed gums and their passage to the periodontal ginglvalis lumen are speculated to fuel both tissue destruction and the development of the flora. The individual contribution to the disease of each bacterial species is difficult to establish and the eventual role of protozoa in the fate of this disease has been ignored.
Following recent scientific findings, we discuss the relevance of these data and propose that the status of E. Periodontitis is a disease leading to alveolar bone destruction and eventually tooth loss. The prevalence of periodontitis is constant among the defined World Health Organization WHO regions, with around one person out of two between 35 and 44 years old Petersen and Ogawa, This prevalence increases with age Demmer and Papapanou, Periodontitis is a handicapping disease, for which the WHO calculated the loss of 3, DALYs Entamoebw life years, a measure of disease burden as the loss of healthy life years in in the world, meaning 0.
Though periodontitis is linked to systemic diseases like diabetes Nascimento et al. The etiology of periodontitis is still unclear and it is classified by the WHO as a non-communicable disease. Some human genetic factors linked to periodontitis were demonstrated Vieira and Albandar, and are still investigated to explain its prevalence in the global population, in conjunction with age Demmer and Papapanou, Modifiable risk factors for the disease were also sought and some parameters have been identified: Beyond pain from wounds, eventual edentulism, and defects in occlusion, the patients experience halitosis Silva et al.
Altogether, these factors may account for their psychological and social distress Lopez et al. Evolution toward gum disease goes through three stages i formation of dental plaque; ii gingivitis, which is an inflammation of the gums due to the dental plaque, and iii periodontitis, in which alveolar bone and fibers that hold the teeth in place are irreversibly damaged. The pathophysiology of the disease is harshly debated, but a consensus was reached about some key points.
First, inflammation is compulsory and prior to bone loss, evidenced by pocket formation [reviewed in Van Dyke ]. Second, the microbial flora in periodontal pockets differs from that observed in healthy sulci Marsh, These paths lead to an inefficient solution dealing with late symptoms without considering the evoked causes of the disease.
The keystone for the improvement of periodontitis management worldwide is a better knowledge of its pathophysiology. Due to the important correlation of periodontitis with the presence of Entamoeba gingivalis in the oral cavity, here, we searched for the facts that can shed light on the question of whether E.
In this review, we summarize existing data on the biology of the amoeba Entamoeba gingivalis and on its potential role as an infectious agent in periodontitis. We aim at highlighting perspectives for new research on the pathophysiology and prophylaxis of this neglected disease. Though the saliva contains low nutrient concentrations and antimicrobial defense systems [reviewed in van ‘T Hof et al. Microorganisms and oral mucosae maintain a mutualistic, resilient symbiotic relationship Rosier et al.
The bacterial ecosystem of healthy sulci is intriguingly similar between individuals and it comprises immotile bacilli and cocci, as seen in microscopy Listgarten,with bacterial species differing from those encountered on the tongue Aas et al. At the tooth surface, in particular in the dental sulcus, nutrients coming from food and cellular debris accumulate and support the survival of bacteria that adhere and colonize the dental enamel. Bacterial flagella, pili, and wall proteins can recruit other bacteria, by co-aggregation Kolenbrander and Celesk, ; Gibbons et al.
Furthermore, the secretion of polysaccharides initiates the formation and organization of a scaffold Jakubovics,while intercellular signaling molecules regulate biofilm development, in particular through a quorum sensing mechanism mediated by different types of messengers, as cyclic di-guanosine monophosphate or LuxS [reviewed in Marsh et al. This intra- and inter-species communication leads to coordination of activities and increases the chances of genetic material transfer.
The resulting dental plaque is an organized biofilm, whose formation is not pathologic Gibbons and Van Houte,though it was thought to be responsible for gingivitis and periodontitis Schultz-Haudt et al. Some bacteria are associated with periodontitis and this led to the proposal of a specific plaque explanation for the disease Loesche, These bacteria group in clusters associated with disease progression Socransky et al. Koch’s postulates are the extreme case of Hill’s criteria for causation Hill, in which infection by a single etiologic agent is the unique parameter influencing the occurrence of the disease Inglis, Thus, the quest for a single pathogen explaining the etiology of periodontitis by itself, following Koch’s postulates, may be in vain.
Contrariwise, periodontitis, as a biofilm disease Schaudinn et al.
Eric Davis Dental – Treatment: Steps To Success
Bacteria are among these parameters and the composition of the microbial communities accurately correlates with clinical outcome Feres et al. Indeed, some species can be efficiently used as markers for diagnosis Meuric et al. Beside changes in its composition, the etamoeba community can harbor changes in its functions, generating a new equilibrium dysbiosis that is possible in the new dental plaque environment Hajishengallis and Lamont, Bacterial entities collaborate and functional changes, such as synergism, are evidenced at the transcriptional level Kirst et al.
Nevertheless, the abundance of some bacterium species is not synonymous for enatmoeba activity Mark Welch et al. This ecology is impacted by the dysbiotic communities, as entamoebba in gingivalsi with deregulated host inflammatory responses Yost et al.
The consequences of dysbiosis were also evidenced in vivo at the systemic level, with metabolic changes linked to diabetes Branchereau et al. While the dental plaque stacks, mineralization leads to formation of tartar deposits, which can cause injury, as well as overhanging restorations or repetitive wounding.
In parallel, the constant gingivaliis of bacterial components and the possible colonization by periodontopathogens can be sensed by the host and can cause chronic inflammation and an initial tissue lesion [reviewed in Kurgan and Kantarci ]. The host takes part in fueling progression to disease by inflammation and active mediators of inflammation resolution improve the disease’s outcome Lee et al.
Resident leukocytes and endothelial cells respond to bacterial biofilms: Neutrophils play a pivotal role in periodontitis Ryder,producing reactive oxygen species ROSwith probable impact dntamoeba the systemic level [reviewed in Wang et al. While the early lesion progresses, other immune cells are recruited, including macrophages, lymphocytes, plasma cells, and mast cells. The inflammation can be visible at the microscopic level, where rete pegs—epithelial projections into the underlying gingivaalis tissue—form in the pocket epithelium and blood vessels proliferate [reviewed in Zoellner et al.
Macrophages are predominant at this stage Dennison and Van Dyke, ; they can derive from circulating monocytes produced in the spleen or be resident macrophages from embryonic origin, like Langerhans cells, with a possible different role during gum inflammation Moughal et al.
In established lesions, adaptive responses take place and lymphocytes are abundantly detected Gemmell et al. Collagen fibers are increasingly altered, leading to a severe tissue remodeling and loosening of the pocket epithelium Payne et al. Thus, greater amounts of dental plaque can accumulate in subgingival locations and aggravate gingivitis, which is considered reversible after elimination of the biofilm, in particular due to the absence of bone and periodontal ligament destruction Ebersole et al.
Left untreated, gingivitis evolves to periodontitis, which is characterized by an inflammatory infiltrate composed of plasma cells, and by degradation of collagen fibers, loss of connective tissue, and bone destruction entanoeba an anaerobic environment Entamoeb et al. Periodontitis results in clinical attachment loss, i. The resulting volume below the gum forms the periodontal pocket, witnessing the breaking down of the initial epithelial attachment, the gingialis of the connective tissues constituting the periodontal entwmoeba, and the lysis of the alveolar bone.
The sulcus depth—the distance between the free gingival margin and the epithelial attachment—is inferior to 3 mm in healthy or gingivitis sites. When superior to 3 mm, periodontitis is suspected and confirmed by inflammation redness and swelling and bleeding on probing.
During periodontitis, the balance between bone resorption and regeneration is displaced: Th17 cells induce osteoclastogenesis Sato et al. In human periodontal lesions, Th17 lymphocytes are abundant Hajishengallis, and the major source of IL Furthermore, osteogenesis is impaired during periodontitis, while bone resorption by osteoclasts is promoted Zhou et al.
Beside the bacteria and human cells, some archaea, viruses, protozoa, and fungi are differentially present in healthy and diseased sites Deng et al. The contributions of sntamoeba different phenomena, as well as lysis by pathogens or other host immune cells, still need to be elucidated to solve the current paradigm of periodontitis physiopathology, in which only some of the players are visible in the game.
Though periodontitis was described since antiquity Langsjoen,its association with parasites has been evidenced only a century ago. The pathogenicity of Entamoeba gingivalis was questioned early Kartulis, and the first systematic study associating it with periodontitis was preliminarily published in Barrett, Furthermore, administration of emetine caused the withdrawal of amoebae and was followed by the cure of pyorrhea in 13 patients Barrett, It is of epistemological importance to underline that systematic studies, some with a low number of participants, about the involvement of Entamoeba netamoeba in periodontitis were countered ginyivalis specialist opinions without formal experimental proofs, as reported by Craig Craig, This controversy led to an almost total abandon of the etiology- and emetine-based therapy, discrediting at the same time its original scientific background.
Further statements about entamieba non-permanent cure were made but were unsupported by scientific data, and incriminating relapses Howitt, However, the possibility of re-infections was completely ignored and casts doubts about the understanding of both pathophysiology gingjvalis epidemiology of the disease at that time.
In parallel, a method for the culture of Gingivxlis.
However, in a single experiment were evaluated the minimum lethal entakoeba MLC, around This underlines that the experimental methodology to study the effect of emetine on E. The conclusions of this paper should thus be considered with caution because this in vitro study did not corroborate the results reported during the treatment of patients, as previously cited.
After this controversy, only a few studies based on the microscopic detection of E. In the cited publications, the prevalence of E. Development of gene amplification by polymerase chain reaction PCR and the sequencing of a gene of E. The first study—using a long amplicon 1.
In the second study, A third study showed a prevalence of Recently, transcriptomics revealed that E. Furthermore, genetic variants of E.
Entamoeba gingivalis in Acute Osteomyelitis of the Mandible
The new clinical characterization of periodontitis Tonetti et al. Altogether, these data suggest entamoeab E. In most species of the genus Entamoebatwo cellular forms have been identified in nature: The survival of these Entamoeba species is ensured by their encystment in response to environmental changes Mi-Ichi et al. However, it is now commonly accepted that E.
Nevertheless, the parasite E. Direct transmission wntamoeba trophozoites to a new host would imply that they are resistant to oxygen, which raises questions about how E. Unfortunately, the complete life cycle of E.