Periodontal Disease Pathology Research Articles

Periodontal disease in down syndrome: Predisposing factors and potential non-surgical therapeutic approaches.

Periodontal diseases (PDs) have been documented to be significantly more prevalent and severe in patients with Down syndrome (DS). Different immunological and microbiological factors contributed to predisposing these patients to progressive and recurrent PDs. The aim of this review was to investigate the altered immunological responses and oral microbiota disorders as well as focus on adjunctive non-surgical methods for the treatment of PDs and its applicability in patients with DS. A literature review was conducted addressing the following topics: (1) the altered immunological responses, (2) orofacial disorders related to DS patients, (3) oral microbiota changing, and (4) adjunctive non-surgical treatment and its efficacy in patients with DS. Due to the early onset of PDs in children with DS, the need for prompt and effective treatment in these patients is essential. So, investigating underlying factors may open a new window to better understand the pathology of PDs in DS people and thus, find better strategies for treatment in such group. Although non-surgical treatments such as photodynamic therapy and probiotic consumption represented acceptable outcomes in different examined patients without DS, data about the application of these convenience and no need for local anesthesia methods in patients with DS is limited.

Mediterranean diet component oleic acid increases protective lipid mediators and improves trabecular bone in a Porphyromonas gingivalis inoculation model.

Therapeutic modulation of bacterial-induced inflammatory host response is being investigated in gingival inflammation and periodontal disease pathology. Therefore, dietary intake of the monounsaturated fatty acid (FA) oleic acid (OA (C18:1)), which is the main component of Mediterranean-style diets, and saturated FA palmitic acid (PA (C16:0)), which is a component of Western-style diets, was investigated for their modifying potential in an oral inoculation model of Porphyromonas gingivalis. Normal-weight C57BL/6-mice received OA- or PA-enriched diets (PA-ED, OA-ED, PA/OA-ED) or normal standard diet for 16 weeks and were inoculated with P. gingivalis/placebo (n=12/group). Gingival inflammation, alveolar bone structure, circulating lipid mediators, and in vitro cellular response were determined. FA treatment of P. gingivalis-lipopolysaccharide-incubated gingival fibroblasts (GFbs) modified inflammatory activation, which only PA exacerbated with concomitant TNF-α stimulation. Mice exhibited no signs of acute inflammation in gingiva or serum and no inoculation- or nutrition-associated changes of the crestal alveolar bone. However, following P. gingivalis inoculation, OA-ED improved oral trabecular bone micro-architecture and enhanced circulating pro-resolving mediators resolvin D4 (RvD4) and 4-hydroxydocosahexaenoic acid (4-HDHA), whereas PA-ED did not. In vitro experiments demonstrated significantly improved differentiation in RvD4- and 4-HDHA-treated primary osteoblast cultures and reduced the expression of osteoclastogenic factors in GF. Further, P. gingivalis infection of OA-ED animals led to a serum composition that suppressed osteoclastic differentiation in vitro. Our results underline the preventive impact of Mediterranean-style OA-EDs by indicating their pro-resolving nature beyond anti-inflammatory properties.

Gingival Parasitic Infections as a Contributor to Periodontitis: Identification and Treatment

Objectives: Parasites play a role in the pathology of periodontal disease with the protozoan Entamoeba gingivalis frequently observed when periodontal disease is present and has been ignored as a contributor to periodontal disease. Identification of the presence of periodontal parasites and how to treat them to eliminate their contribution to periodontal disease will be addressed. Methods: The first phase of therapy is reconstituting a normal commensal biofilm with minimal supragingival calculus removal to limit potential for the parasites to invade the soft tissue lining of the pocket and potentially spread related to the bleeding capillaries. At the fourth month, a systemic antiparasitic medication (metronidazole) is added. The second phase of therapy consists of four monthly subgingival calculus removal using sonic or ultrasonic instruments. Microscopic evaluation is used to confirm the absence of parasites. Results: The Bonner Method is nonsurgical. Pocket closure and osseous regrowth, without supplemental grafting help confirm healing and continued use of the homecare regime allow the patient to maintain gingival health long-term. Microbiota microscopic examination at every visit during active treatment confirms healing and elimination of the parasites. Conclusions: Patient who have traditionally avoided dental treatment or have experienced traditional surgery in the past easily accept antiparasitic treatment, which is reached from clinical and microscopic co-examination. Many of these patients are seeking an alternative to traditional surgery and are more comfortable with the basics behind the protocol once they have seen their biofilm under video from their microscopic sampling. Clinical significance: The subject of this article has clinical relevance, as parasites are an unrecognized contributor to periodontal disease that is frequently not identified or understood. This article discusses its clinical relevance, how to identify its presence and treatment to eliminate the parasite as part of periodontal treatment. The authors feel that this will have relevance to dental hygienists as they are the practitioner who would be first to identify its presence and provide treatment in the dental practice.

The Influence of Periodontal Treatment on Salivary Visfatin Biomarker levels in Non-obese Indian Population with Different forms of Periodontal Disease- A Clinico-Biochemical Study

The ability to correctly diagnose and institute effective periodontal therapy is essential to control periodontal diseases. Rapid advances in diagnostic research are moving towards methods whereby periodontal disease risk can be identified and quantified by measuring biomarkers. This study investigated the effect of Non-Surgical Periodontal Treatment (NSPT) on clinical indices and salivary levels of visfatin in subjects with increasing severity of the periodontal disease. This interventional clinical trial was performed on 60 systemically healthy male and female subjects (20 to 50 years) who were categorised into Group-1, Twenty subjects with healthy periodontium, Group-2, Twenty subjects with generalized moderate gingivitis, and Group-3 (20 subjects with moderate to severe periodontitis (Stage III according to the new classification of periodontal diseases). The visfatin levels were measured in unstimulated saliva by using standard EnzymeLinked Immunosorbent Assay (ELISA) technique at baseline and six weeks after NSPT. The salivary visfatin levels were highest in Group-3 (38.22±3.38 ng/ml) followed by Group - 2 (26.66±2.24 ng/ml) and Group-1 (25.60±2.19 ng/ml) at baseline. After NSPT statistically significant reduction in salivary visfatin levels (p<0.001) in Groups -2 and 3 were seen. Visfatin levels at baseline were almost equivocal in normal weight and overweight subjects, irrespective of body mass index and showed a statistically significant reduction in salivary visfatin levels in both groups six weeks after NSPT (p<0.001). The present study suggests that salivary visfatin is a strong contributor in the pathology of periodontal disease and can be used as its diagnostic/therapeutic biomarker.

Influence of Gestational Hormones on the Bacteria-Induced Cytokine Response in Periodontitis.

Periodontitis is an inflammatory disease that affects the supporting structures of teeth. The presence of a bacterial biofilm initiates a destructive inflammatory process orchestrated by various inflammatory mediators, most notably proinflammatory cytokines, which are upregulated in the gingival crevicular fluid, leading to the formation of periodontal pockets. This represents a well-characterized microbial change during the transition from periodontal health to periodontitis; interestingly, the gestational condition increases the risk and severity of periodontal disease. Although the influence of periodontitis on pregnancy has been extensively reviewed, the relationship between pregnancy and the development/evolution of periodontitis has been little studied compared to the effect of periodontitis on adverse pregnancy outcomes. This review is aimed at summarizing the findings on the pregnancy-proinflammatory cytokine relationship and discussing its possible involvement in the development of periodontitis. We address (1) an overview of periodontal disease, (2) the immune response and possible involvement of proinflammatory cytokines in the development of periodontitis, (3) how bone tissue remodelling takes place with an emphasis on the involvement of the inflammatory response and metalloproteinases during periodontitis, and (4) the influence of hormonal profile during pregnancy on the development of periodontitis. Finally, we believe this review may be helpful for designing immunotherapies based on the stage of pregnancy to control the severity and pathology of periodontal disease.

Vascular Changes and Hypoxia in Periodontal Disease as a Link to Systemic Complications.

The hypoxic microenvironment caused by oral pathogens is the most important cause of the disruption of dynamic hemostasis between the oral microbiome and the immune system. Periodontal infection exacerbates the inflammatory response with increased hypoxia and causes vascular changes. The chronicity of inflammation becomes systemic as a link between oral and systemic diseases. The vascular network plays a central role in controlling infection and regulating the immune response. In this review, we focus on the local and systemic vascular network change mechanisms of periodontal inflammation and the pathological processes of inflammatory diseases. Understanding how the vascular network influences the pathology of periodontal diseases and the systemic complication associated with this pathology is essential for the discovery of both local and systemic proactive control mechanisms.

Inflamm-Aging-Related Cytokines of IL-17 and IFN-γ Accelerate Osteoclastogenesis and Periodontal Destruction

Periodontal disease (PD), as an age-related disease, prevalent in middle-aged and elderly population, is characterized as inflammatory periodontal tissue loss, including gingival inflammation and alveolar bone resorption. However, the definite mechanism of aging-related inflammation in PD pathology needs further investigation. Our study is aimed at exploring the effect of inflamm-aging-related cytokines of interleukin-17 (IL-17) and interferon-γ (IFN-γ) on osteoclastogenesis in vitro and periodontal destruction in vivo. For receptor activator of nuclear factor-κB ligand- (RANKL-) primed bone marrow macrophages (BMMs), IL-17 and IFN-γ enhanced osteoclastogenesis, with the expression of osteoclastogenic mRNA (TRAP, c-Fos, MMP-9, Ctsk, and NFATc1) and protein (c-Fos and MMP-9) upregulated. Ligament-induced rat models were established to investigate the role of IL-17 and IFN-γ on experimental periodontitis. Both IL-17 and IFN-γ could enhance the local inflammation in gingival tissues. Although there might be an antagonistic interaction between IL-17 and IFN-γ, IL-17 and IFN-γ could facilitate alveolar bone loss and osteoclast differentiation.

Domestic prophylactic agents in maintaining the dental health of the elderly

Goal. To investigate dental health and oral microbiota in elderly people who use domestic care products after the completion of their sanitation.Material and methods. The prevalence and intensity of the course of dental caries, periodontal pathology, pathology of the oral mucosa, as well as the microbiota in 96 people aged 61 to 73 years were studied using conventional research methods in dentistry in elderly patients who visited a dentist for a year according to the appealability (group 1) or were under dynamic supervision and regularly carried out individual oral hygiene with the help of domestic ASEPTA products (group 2).Results. Individual prophylactic and hygienic measures for the care of the oral cavity, regularly carried out by elderly patients of group 2, significantly improved their dental health, contributed to the secondary prevention of periodontal diseases and a significant reduction in periodontal pathogens in the oral cavity.Conclusion. Elderly patients who are regularly observed by a dentist with a complex of measures for the primary and secondary prevention of dental diseases carried out 2 times a year, as well as with their proper adherence to oral care, it is possible to achieve effective treatment of the pathology of hard dental tissues, remission of inflammatory pathology of periodontal disease, and also good oral hygiene, which has a positive effect on their quality of life.

Effect of Periodontal Disease-associated Bacteria on the Formation of Dental Calculus: An In Vitro Study

Aim:To investigate whether bacteria that play a major role in periodontal disease pathology and in the formation of dental plaque also affect the formation of dental calculus, which is a predisposing factor for the initiation and progression of periodontal diseases.Materials and Methods:This was an in vitro study, and cultures of bacteria were obtained from the American Type Culture Collection and Department of Biology, Faculty of Science, Atatürk University. Young cultures of bacteria of Streptococcus mutans ( S. mutans), Streptococcus sanguinis ( S. sanguinis), Streptococcus gordonii ( S. gordonii), Aggregatibacter actinomycetemcomitans ( A. actinomycetemcomitans), Porphyromonas gingivalis ( P. gingivalis), Fusobacterium nucleatum ( F. nucleatum), and Corynebacterium matruchotii ( C. matruchotii) were prepared in media containing their specific enriching factors. B2 solid, B4 solid, and B2 liquid media were used to determine active calcification, whereas the mineral salt basal (MSB) medium was used to observe passive calcification. Calcification in the media was measured under light microscopy and in MSB using a spectrophotometer and was recorded as the percent transmittance.Results:S. mutans, S. sanguinis, and S. gordonii showed calcification in the B2 medium. S. mutans, S. sanguinis, S. gordonii, and C. matruchotii demonstrated calcification in MSB. A. actinomycetemcomitans, P. gingivalis, and F. nucleatum did not show any calcification.Conclusions:It was concluded that streptococci present in dental plaque take part in the formation of dental calculus, whereas periodontopathogens have no role in the formation of dental calculus.

Treatment of Porphyromonas gulae infection and downstream pathology in the aged dog by lysine-gingipain inhibitor COR388.

COR388, a small‐molecule lysine‐gingipain inhibitor, is currently being investigated in a Phase 2/3 clinical trial for Alzheimer's disease (AD) with exploratory endpoints in periodontal disease. Gingipains are produced by two species of bacteria, Porphyromonas gingivalis and Porphyromonas gulae, typically associated with periodontal disease and systemic infections in humans and dogs, respectively. P. gulae infection in dogs is associated with periodontal disease, which provides a physiologically relevant model to investigate the pharmacology of COR388. In the current study, aged dogs with a natural oral infection of P. gulae and periodontal disease were treated with COR388 by oral administration for up to 90 days to assess lysine‐gingipain target engagement and reduction of bacterial load and downstream pathology. In a 28‐day dose‐response study, COR388 inhibited the lysine‐gingipain target and reduced P. gulae load in saliva, buccal cells, and gingival crevicular fluid. The lowest effective dose was continued for 90 days and was efficacious in continuous reduction of bacterial load and downstream periodontal disease pathology. In a separate histology study, dog brain tissue showed evidence of P. gulae DNA and neuronal lysine‐gingipain, demonstrating that P. gulae infection is systemic and spreads beyond its oral reservoir, similar to recent observations of P. gingivalis in humans. Together, the pharmacokinetics and pharmacodynamics of COR388 lysine‐gingipain inhibition, along with reduction of bacterial load and periodontal disease in naturally occurring P. gulae infection in the dog, support the use of COR388 in targeting lysine‐gingipain and eliminating P. gingivalis infection in humans.

Extracellular RNAs in periodontopathogenic outer membrane vesicles promote TNF-α production in human macrophages and cross the blood-brain barrier in mice.

Among the main bacteria implicated in the pathology of periodontal disease, Aggregatibacter actinomycetemcomitans (Aa) is well known for causing loss of periodontal attachment and systemic disease. Recent studies have suggested that secreted extracellular RNAs (exRNAs) from several bacteria may be important in periodontitis, although their role is unclear. Emerging evidence indicates that exRNAs circulate in nanosized bilayered and membranous extracellular vesicles (EVs) known as outer membrane vesicles (OMVs) in gram-negative bacteria. In this study, we analyzed the small RNA expression profiles in activated human macrophage-like cells (U937) infected with OMVs from Aa and investigated whether these cells can harbor exRNAs of bacterial origin that have been loaded into the host RNA-induced silencing complex, thus regulating host target transcripts. Our results provide evidence for the cytoplasmic delivery and activity of microbial EV-derived small exRNAs in host gene regulation. The production of TNF-α was promoted by exRNAs via the TLR-8 and NF-κB signaling pathways. Numerous studies have linked periodontal disease to neuroinflammatory diseases but without elucidating specific mechanisms for the connection. We show here that intracardiac injection of Aa OMVs in mice showed successful delivery to the brain after crossing the blood-brain barrier, the exRNA cargos increasing expression of TNF-α in the mouse brain. The current study indicates that host gene regulation by microRNAs originating from OMVs of the periodontal pathogen Aa is a novel mechanism for host gene regulation and that the transfer of OMV exRNAs to the brain may cause neuroinflammatory diseases like Alzheimer's.-Han, E.-C., Choi, S.-Y., Lee, Y., Park, J.-W., Hong, S.-H., Lee, H.-J. Extracellular RNAs in periodontopathogenic outer membrane vesicles promote TNF-α production in human macrophages and cross the blood-brain barrier in mice.

Keratinocyte-specific ablation of protease-activated receptor 2 prevents gingival inflammation and bone loss in a mouse model of periodontal disease

Chronic periodontitis is characterised by gingival inflammation and alveolar bone loss. A major aetiological agent is Porphyromonas gingivalis, which secretes proteases that activate protease-activated receptor 2 (PAR2 ). PAR2 expressed on oral keratinocytes is activated by proteases released by P.gingivalis, inducing secretion of interleukin 6 (IL-6), and global knockout of PAR2 prevents bone loss and inflammation in a periodontal disease model in mice. To test the hypothesis that PAR2 expressed on gingival keratinocytes is required for periodontal disease pathology, keratinocyte-specific PAR2 -null mice were generated using K14-Cre targeted deletion of the PAR2 gene (F2rl1). These mice were subjected to a model of periodontitis involving placement of a ligature around a tooth, combined with P.gingivalis infection ("Lig+Inf"). The intervention caused a significant 44% decrease in alveolar bone volume (assessed by microcomputed tomography) in wildtype (K14-Cre:F2rl1wt/wt ), but not littermate keratinocyte-specific PAR2 -null (K14-Cre:F2rl1fl/fl ) mice. Keratinocyte-specific ablation of PAR2 prevented the significant Lig+Inf-induced increase (2.8-fold) in the number of osteoclasts in alveolar bone and the significant up-regulation (2.4-4-fold) of the inflammatory markers IL-6, IL-1β, interferon-γ, myeloperoxidase, and CD11b in gingival tissue. These data suggest that PAR2 expressed on oral epithelial cells is a critical regulator of periodontitis-induced bone loss and will help in designing novel therapies with which to treat the disease.

SOME ASPECTS OF THE EATIOLOGY OF PARODONTUS DISEASES. (LITERATURE REVIEW)

The review of the scientific literature is devoted to the topical issues of studying the etiology of periodontal diseases, which are one of the most common and complex pathologies of the maxillofacial region.
 Analysis of recent studies proves a stable relationship between the development of periodontal diseases and disorders in the immune system, the neurohumoral system, metabolic disorders, genetic predisposition, and so on. The article presents the data obtained in the course of studying the literature on the role of disorders in the functioning of individual organs (gastrointestinal tract, liver, lungs, heart, and urinary system) in the development of chronic periodontal diseases. The article notes that the anatomical and physiological proximity of the periodontal and digestive tract tissues, the generality of innervation and humoral regulation create prerequisites for the involvement of periodontal disease in the pathological process in diseases of the gastrointestinal tract. One of the main etiological factors in the development of inflammatory diseases of the gastrointestinal tract and periodontium is Helicobacter pylori, which is found in the loci of the oral cavity: in the oral and gingival fluid, on the mucous membrane of the tongue and cheeks, and in the periodontal pockets.
 It is pointed out that the liver also occupies a special place in the development of periodontal diseases, which is explained by the performance of its significant functions for the human body: regulatory, metabolic, antitoxic and other.
 There is evidence that the pathology of periodontal disease plays a leading role in the structure of dental diseases in patients with chronic obstructive pulmonary diseases, which is clinically manifested by symptoms of generalized periodontitis of the І-ІІ degrees of development and its complications - partial or complete secondary adentia, and with tooth preservation - defects in dental series and violations of occlusion, function, aesthetics.
 Scientists suggest a general biological mechanism for the development of generalized periodontitis and cardiovascular diseases, linking the development of periodontal diseases in patients with cardiovascular pathology with microcirculatory disorders.
 The dependence of the severity of inflammatory changes in the periodontal tissues on the disturbances of salt metabolism in urolithiasis is proved.
 The data obtained indicate that diseases of the internal organs contribute to the structural damage of periodontal tissues and they are a risk factor for periodontal diseases, which necessitate the presence of not only theoretical knowledge and practical skills in dentistry, but also their awareness of the features and clinical manifestations of somatic pathology. An urgent and justified step in the treatment of periodontal diseases is also the involvement in the process of rendering complex dental care to internist doctors capable of quickly and qualitatively assessment the condition of the internal organs and the basic systems of the patient's body.

КЛІНІЧНА ЕФЕКТИВНІСТЬ ЗАСТОСУВАННЯ ФІТОПРЕПАРАТУ «РЕСВЕРАЗИН» В КОМПЛЕКСНОМУ ЛІКУВАННІ ГЕНЕРАЛІЗОВАНОГО ПАРОДОНТИТУ

Захворювання пародонта – сьогодні одне із найпоширеніших уражень організму людини. За даними ВООЗ (1990), від 55 до 98 % дорослого населення планети має патологію пародонта, найвищий рівень захворюваності зареєстровано в осіб 15–19 років (55–89 %) та 35–44 років (65–98 %) [1, 3, 6]. Висока поширеність, несприятливий вплив вогнищ пародонтальної інфекції на стан порожнини рота та організм у цілому, високий рівень ускладнень, пов’язаних із функціональними та морфологічними порушеннями внаслідок втрати зубів, – все це визначає актуальність даної проблеми.Мета дослідження – оцінити клінічну ефективність препарату “Ресверазин” у складі комплексного лікування генералізованого пародонтиту.Матеріали і методи. У дослідженні взяли участь 43 пацієнти, хворі на хронічний генералізований пародонтит. Оцінку стану пародонта проводили за клінічними ознаками. Для оцінки гігієнічного стану порожнини рота використовували індекси Green–Wermillion, ОНІ-S, Silness–Loe, Stallard, пародонтологічні індекси: РМА, ПІ, індекс кровоточивості за Мuhlleman. Визначення і підрахунок індексів проводили за загальноприйнятими методиками. Пацієнтам основної групи в комплексній терапії призначали препарат “Ресверазин” по 1 капсулі 2 рази на добу. Курс лікування становив 2 місяці.Результати дослідження та їх обговорення. Дані клінічних досліджень, які ми отримали, послугували обґрунтуванням для впровадження в медичну стоматологічну практику лікування генералізованого пародонтиту (ГП) фітопрепаратом “Ресверазин”. Включення до комплексної терапії хворих на пародонтит препарату “Ресверазин” сприяло підвищенню ефективності проведеного етіотропного, патогенетичного та симптоматичного лікування хворих, що забезпечило клінічно виражені ознаки стабілізації пародонтиту та швидший перехід ГП у стадію ремісії. Позитивний клінічний результат отриманий за основними критеріями ефективності, які заключались у зменшенні симптомів запалення – гіперемії, набряку та кровоточивості міжзубних сосочків і маргінальної частини ясен. Тенденція до зменшення ознак запалення за клінічними, суб’єктивними даними, підтвердилась позитивною динамікою показника поширеності запаленнятканин  пародонта (РМА). Зниження значення інтегративного пародонтального індексу відбувається переважно за рахунок зменшення тяжкості симптоматичного гінгівіту та глибини пародонтальних кишень. У результаті проведеного лікування настає нормалізація функціональних адаптаційно-компенсаторних реакцій, що підтверджується нормалізацією показників – гігієнічними індексами Green–Wermillion, ОНІ-S, Silness–Loe, Stallard та пародонтальними індексами: папілярно-маргінально-альвеолярним (РМА), індексом кровоточивості за Muhlleman, пародонтальним індексом (ПІ).Висновки. Результати клінічного дослідження свідчать про необхідність застосування фітопрепаратів, зокрема фітопрепарату “Ресвератрол”, із протизапальною, антиангіогенною, імунотропною, антиоксидантною дією в комплексному лікуванні хворих на генералізований пародонтит.

Metabolic control and periodontal treatment decreases elevated oxidative stress in the early phases of type 1 diabetes onset

ObjectiveRecently, increasing concern has been focused on the contribution of oxidative stress in the pathology of periodontal disease and diabetes mellitus. Firstly, the present study aimed to analyze gingival crevicular fluid (GCF), salivary, and serum oxidative status in children with type 1 diabetes mellitus (T1DM) at diagnosis and systemically healthy children with and without gingivitis. Additionally, the diabetic patients were reevaluated after diabetes and periodontal treatment. DesignThe study groups were composed of 32 T1DM patients at diagnosis, and age- and gender-matched thirty-six systemically healthy children with (G) and without (H) gingivitis. The diabetic patients who took insulin therapy (1.5 units/kg/day totally) and periodontal treatment (oral hygiene education with professional scaling) were reevaluated after 3 months. The levels of total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were recorded. ResultsGCF, salivary, and serum OSI were elevated in group T1DM compared to the other groups at baseline (p<0.05), and decreased in group T1DM at reevaluation compared to baseline (p<0.05). GCF OSI was positively correlated with periodontal clinical parameters (p<0.05). Glycated hemoglobin was positively correlated with GCF TOS (r=0.302, p=0.007), GCF OSI (r=0.346, p=0.002), salivary TOS (r=0.326, p=0.046), and serum TOS (r=0.239, p=0.044). ConclusionThe instability in the oxidative status that accompanies diabetes may be considered a significant pathogenic factor of diabetes-related periodontal inflammation.

РОЛЬ МІКРООРГАНІЗМІВ, ВИДІЛЕНИХ ІЗ ПАРОДОНТАЛЬНИХ КИШЕНЬ В ПАТОГЕНЕЗІ ГЕНЕРАЛІЗОВАНОГО ПАРОДОНТИТУ У ОСІБ З ЛЯМБЛІОЗНОЮ ІНВАЗІЄЮ

Питання етіопатогенезу генералізованого пародонтиту хронічного перебігу у осіб з паразитарною інвазією до теперішнього часу залишаються маловивченими.Метою цієї роботи було вивчення ролі мікробів, виділених з пародонтальних кишень, у розвитку генералізованого пародонтиту в осіб з лямбліозом.Матеріали і методи. Було обстежено 120 хворих на генералізований пародонтит І–ІІ ступеня тяжкості хронічного перебігу на тлі лямбліозу (основна група). Групу порівняння склали 90 осіб з ГП І–ІІ ступенів тяжкості хронічного перебігу без лямбліозної інвазії. Контрольна група представлена 30 особами без патології пародонта і хронічної патології інших систем, які в період обстеження вважалися практично здоровими.Мікробіологічні дослідження включали виділення та ідентифікацію мікроорганізмів з використанням техніки аеробного і анаеробного культивування.Статистичну обробку матеріалів проводили з використанням методів математичної статистики для аналізу отриманих даних.Результати. Встановлено, що у мікроорганізмів, які колонізують пародонтальні кишені у хворих на генералізований пародонтит І–ІІ ступенів тяжкості на тлі лямбліозу, присутні антигени тканинних структур пародонта.Висновок. Мікроорганізми пародонтальних кишень є не тільки індукторами банального запалення в тканинах пародонта внаслідок їх патогенних властивостей (токсиноутворення, продукції ферментів агресії тощо), але й виступають потужним фактором, що модифікує силу і спрямованість вектора імунної реакції. Імунна реакція, яка за своєю природою і суттю є виключно захисним механізмом організму, здатна під впливом мікробів, що експресують тканинні антигени мімікрії, перетворюватися на чинник агресії проти власних тканин.

The inflammasome and danger molecule signaling: at the crossroads of inflammation and pathogen persistence in the oral cavity.

Inflammasomes are an oligomeric assembly of multiprotein complexes that activate the caspase-1-dependent maturation and the subsequent secretion of inflammatory interleukin-1beta and interleukin-18 cytokines in response to a 'danger signal' in vertebrates. The assessment of their significance continues to grow rapidly as the complex biology of various chronic inflammatory conditions is better dissected. Increasing evidence strongly links inflammasomes and host-derived small 'danger molecule ATP' signaling with the modulation of the host immune response by microbial colonizers as well as with potential altering of the microbiome structure and intermicrobial interactions in the host. All of these factors eventually lead to the destructive chronic inflammatory disease state. In the oral cavity, a highly dynamic and multifaceted interplay takes place between the signaling of endogenous danger molecules and colonizing microbes on the mucosal surfaces. This interaction may redirect the local microenvironment to favor the conversion of the resident microbiome toward pathogenicity. This review outlines the major components of the known inflammasome complexes/mechanisms and highlights their regulation, in particular, by oral microorganisms, in relation to periodontal disease pathology. Better characterization of the cellular and molecular biology of the inflammasome will probably identify important potential therapeutic targets for the treatment and prevention of periodontal disease, as well as for other debilitating chronic diseases.

Is there a link between carbamylation and citrullination in periodontal disease and rheumatoid arthritis?

The remarkable similarity in inflammatory response and pathology of periodontal disease and rheumatoid arthritis has been recognized for several decades. However, how these two disease may be interrelated has been less clear. During the pathogenesis of rheumatoid arthritis there is a preclinical immunological phase which precedes the clinical manifestation of rheumatoid arthritis. During this phase serum autoantibodies appear many years before the clinical signs and symptoms of rheumatoid arthritis become apparent. To date, the two best studied autoantibodies have been rheumatoid factor and anti-citrullinated protein antibodies (ACPA). Of these the production of ACPA has been considered very important due to their high predictive value in future manifestation of rheumatoid arthritis. Citrullination is a common post-translational modification of proteins based on the enzymatic conversion of arginine into citrulline. Extra-articular citrullination and production of ACPA, as a priming immunological experience, is well documented in many tissues including the inflamed gingival tissues associated with periodontal disease. More recently, carbamylation of proteins has also been implicated in the pathogenesis of rheumatoid arthritis in a manner similar to citrullination. Carbamylation is a post translational modification of proteins by an enzyme-independent modification of lysine residues against which autoantibodies are subsequently induced. In this article we hypothesise that, like citrullination, carbamylation of proteins and associated antibody production during the gingival inflammation associated with gingivitis and periodontitis may play a role in the pathogenesis of rheumatoid arthritis.

Transforming Growth Factor Beta 1 and Vascular Endothelial Growth Factor Levels in the Pathogenesis of Periodontal Disease

Periodontal disease is characterized by inflammation and bone loss. The balance between inflammatory mediators and their counter-regulatory molecules may be fundamental for determining the outcome of immune pathology of periodontal disease. Cytokines play crucial roles in the maintenance of tissue homeostasis, a process which requires a delicate balance between anabolic and catabolic activities. In particular, two families of growth factors-such as transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor (VEGF) are thought to play important roles in modulating the proliferation and/or migration of structural cells involved in inflammation and regulation of immune responses. The aim of this work was to analyze gingival samples and periodontal tissue specimens collected from thirty-eight patients with chronic periodontal disease and from forty healthy individuals, in order to detect the expression and distribution of TGF-β1 and VEGF between the two groups. TGF-β1 and VEGF expression levels were detected using immunohistochemical analysis and computer-assisted morphometric analysis. The findings presented here suggest that biomarker such as TGF-β1 and VEGF have an important regulating role in the orchestration of the immune response, which in turn influence the outcome of disease establishment and evolution.

Immunohistochemical analysis of TGF-β1 and VEGF in gingival and periodontal tissues: A role of these biomarkers in the pathogenesis of scleroderma and periodontal disease

Periodontal disease is characterized by inflammation and bone loss. The balance between inflammatory mediators and their counter-regulatory molecules may be fundamental for determining the outcome of the immune pathology of periodontal disease. Transforming growth factor-β (TGF-β) and vascular endothelial growth factor (VEGF) represent a family of polypeptide proteins involved in the inflammation and regulation of immune responses, especially in rheumatic disease. The relationship between these growth factors and periodontitis has resulted in a new field of osteoimmunology and provides a context for better understanding the pathogenesis of periodontal disease. Therefore, the aim of this study was to compare the protein expression profile of these inflammatory mediators in 90 patients divided in three groups: healthy control, chronic periodontitis and in rheumatic disease, scleroderma. The findings presented here highlight that biomarkers, such as TGF-β1 and VEGF, play a key role in the evolution of the immune response, which in turn influences the outcome of disease establishment.