PDF | An year-old woman presented with osteonecrosis of the mandible Entamoeba gingivalis is one of seven Entamoeba species that. PDF | Periodontitis is a public health issue, being one of the most prevalent PCR reactions for Entamoeba gingivalis detection with 40 pg DNA matrix from. Entamoeba gingivalis was the only protozoa found in the oral cavities This study describes for the first time the findings of E. gingivalis in the.
|Language:||English, Spanish, Arabic|
|ePub File Size:||25.85 MB|
|PDF File Size:||11.11 MB|
|Distribution:||Free* [*Sign up for free]|
ORIGINAL ARTICLE. Entamoeba gingivalis – prevalence and correlation with dental caries in children from rural and urban regions of Lublin. Entamoeba gingivalis is an opportunistic Amoebozoa and is the first amoeba in humans to be . Create a book · Download as PDF · Printable version. Entamoeba gingivalis (Fig. ) is cosmopolitan in distribution, commonly found in the tartar and debris associated with the gingival tissues of the mouth.
Entamoeba gingivalis Gros, Entamoeba gingivalis from aggressive periodontal disease patient biofilm using phase contrast microscope x. It is recognizable through its dense core in the middle, formed by a central point encircled by a circular halo and surrounded by bigger phagosomes inside a greyish cytoplasm. Entamoeba gingivalis is an opportunistic Amoebozoa [ citation needed ] reported by some as an effect of disease; not a cause [hence status as a commensal]    and is the first amoeba in humans to be described. It is found in the mouth  inside the gingival pocket biofilm near the base of the teeth, and in periodontal pockets. Only the trophozoites are formed and the size is usually 20 micrometers to micrometers in diameter. Entamoeba gingivalis have pseudopodia that allow them to move quickly and phagocytise the nucleus of polynuclear neutrophils by exonucleophagy in periodontal disease. There are numerous food vacuoles , which consists mostly of phagocitised PMN nucleus, blood cells and bacteria.
Abstract Background: It was shown that two parasites of Entamoeba gingivalis E. This study was designed to evaluate the prevalence of these parasites in oral cavity of patients with periodontal disease and in healthy population in Shiraz, Southern Iran. Materials and Methods: A total of 50 patients with periodontal disease case group and 50 subjects with healthy gingiva control group entered in the present study.
A questionnaire recorded general health, smoking habits, and any history of antibiotic consumption during the last six months for each patient.
In the case group, saliva was collected by sterile swab and the gingival crevicular fluid by the paper point. The plaque and calculi were collected by sterile curette and scaler. In the control group, saliva and gingival crevicular fluid were collected and sent to laboratory for further studies.
Results: In the case group, nine patients were infected, six with E. Seven patients had mobility of the teeth, one patient was smoker and five had previous history of antibiotic consumption. In the control group, only one subject was infected with E. Conclusion: Parasitic infections are relatively common in patients with periodontal disease. It seems that follow-up of instructions are essential in control of parasitic infection in Southern Iran.
Prevalence of oral Entamoeba gingivalis and Trichomonas tenax in patients with periodontal disease and healthy population in Shiraz, southern Iran. Several studies were undertaken in relation to prevalence of T.
This organism has a small round nucleus with a central karyosome and fine granular cytoplasm. The occurrence of E. A total of 50 aged-matched years old patients 29 females and 21 males with periodontal disease confirmed radiographically and clinically periodontal pocket, calculus, swelling and change in consistency and color of the gingiva were considered as case group. A total of 50 patients aged between years 26 females and 24 males without any periodontal disease and healthy gingiva pink in color, normal shape, and consistency were also selected as control group.
In both groups, saliva was collected by sterile swab and the gingival crevicular fluid by paper point and all specimens were put in the containers. In the case group, the plaque and calculi were collected by sterile curette and scaler.
As aging is a risk factor for the 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 pocket 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. Keywords: Entamoeba gingivalis, periodontitis, gingivitis, inflammation, parasitic infection, infectious disease Introduction: a disease with underestimated impact 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 Disability-adjusted 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: smoking Eke et al.
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. Microbiology of periodontitis: the bacterial paradigm 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.
Thus, P. 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. 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 bacterial 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 their activity Mark Welch et al. This ecology is impacted by the dysbiotic communities, as evidenced in vitro 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.
Immuno-pathological processes TOWARD periodontitis 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 presence 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: vascular permeability increases and interleukin 8 attracts neutrophils to the affected tissues Tonetti et al. Neutrophils play a pivotal role in periodontitis Ryder, , producing reactive oxygen species ROS , with probable impact at 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 connective 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 in an anaerobic environment Mettraux et al. Periodontitis results in clinical attachment loss, i.