Introduction: The relationship between periodontal diseases and atherosclerosis is addressed in this article. Both these diseases have an inflammatory basis. Because periodontal disease is a risk factor for developing atherosclerotic vascular disease, diagnosis of the former is important. Particular attention must be paid to patients who have periodontal disease with other risk factors for atherosclerotic vascular disease. Recommendations managing these patients have been made included. The aim: The paper is aimed at familiarization of broad medical public with the presence of the relationship between diseases of periodontal tissues and atherosclerosis. Materials and methods: A thorough comprehensive analysis and generalization of scientific achievements elucidated in the fundamental and periodical publications, relating to diseases of the periodontal tissues and atherosclerosis, has been carried out. Review: The article consists of many researchers regarding the prevalence and intensity of periodontal tissue diseases in people of all ages. Problems associated with the state of periodontal tissues in people under study as dentists and general practitioners. Proven role in the pathogenesis of inflammatory diseases of the periodontal tissues in people with atherosclerosis. In the modern concept of the etiology and pathogenesis of periodontal diseases in people is extremely important role for the immune system and resistance to periodontal bacterial invasion. Analyzed common changes important for pathogenesis of periodontal tissue diseases and atherosclerosis. Conclusions: Consequently, recent studies have shown a clear, directly proportional relationship between periodontal tissue diseases and atherosclerosis, but mechanisms for their development and interaction are not fully disclosed.
The aim: To study the consequences of temporomandibular joint injury and efficacy of arthrocentesis for treatment of post-traumatic internal temporoman¬dibular disorders. Materials and methods: 24 patients who experienced trauma history in the head without jaw fractures underwent CT, ultrasound and/or MRI. TMJ ar¬throcentesis was performed according to a modified method of D. Nitzan (1991) under local anesthesia by means of blockade of the peripheral branch of the auricular-temporal nerve on the background of intravenous sedation. Results: The ages of the patients varied between 18 and 44 years, and mean was 32,58 years. The causes of trauma were diverse, as traffic accident – 3 (12,5%), assault 12 (50%), hit by materials 3 (12, 5%), and fall-down 6 (25%). According to clinical and radiological signs after traumatic temporomandibular disorders, patients were divided into two groups according to Wilkes classification (1989): 13 patients with stage II (early-middle) and 11 - with stage III (middle).The control ultrasound and MRI carried out 3-6 months after arthrocentesis showed no signs of hemarthrosis in 84.61% of patients with intra-articular disorders of the second degree, and in 72.72% of patients with internal disorders of the third degree, the position and function of the articular disc was restored. Conclusions: Arthrocentesis with TMJ lavage is a minimally invasive surgical manipulation that has proven itself in temporomandibular disorders of traumatic origin, in particular after fractures of the articular process of the mandible.
The purpose of the study was to analyze professional literature sources devoted to the influence of homocysteine on the development of vascular disorders. The role of homocysteine as a biomarker of vascular pathology is considered. Materials and methods. Bibliosemantic and analytical methods were used in the study. The analysis of the specialized literature (47 sources) was carried out using information in the scientific-metric databases MEDLINE/PubMed, Scopus and Google Scholar. Results and discussion. Homocysteinemia is a pathological condition associated with quite serious consequences for the body; the endothelium of vessels suffers mostly: systemic endothelial dysfunction develops (including disruption of the synthesis and exchange of the endothelium-relaxing factor – nitric oxide), oxidative stress, activation of platelet aggregation, hypercoagulation occurs (due to a decrease in the activity of heparin, thrombomodulin and an increase in the activity of thromboxane A2). The prevalence of hyperhomocysteinemia in Ukraine is quite high and reaches 10% among healthy adults, 2% among young people and adolescents, from 13% to 43% in patients with cardiovascular pathology. The C677T polymorphism of the methylenetetrahydrofolate reductase gene is widespread among the population of Ukraine (40.7%). Researchers believe that hyperhomocysteinemia is an independent and modifiable risk factor for vascular pathology. Conclusion. Homocysteine is recognized as one of the markers of vascular pathology. Scientists consider the activation of oxidative stress, damage to the endothelium, stimulation of the proliferation of smooth muscle cells, and pro-inflammatory effects to be the main mechanisms of vascular damage in hyperhomocysteinemia. The described pathological changes are accompanied by a violation of the regulation of vascular tone, mostly due to a decrease in the synthesis of nitric oxide. Unbalanced synthesis of nitric oxide causes and potentiates oxidative stress, the processes of atherothrombogenesis. The professional literature presents enough scientific data that convincingly prove the role of homocysteine in the development of cardiovascular and neurological pathology. However, there is a small number of studies devoted to the relationship between hyperhomocysteinemia and periodontal diseases, and the pathogenetic mechanisms of the influence of hyperhomocysteinemia on the development of vascular disorders in coronavirus disease are not fully disclosed
The purpose of the study was to establish pathogenetic mechanisms, in particular, disorders of purine and protein metabolism of blood serum, which can cause increased susceptibility of gout patients to periodontal diseases, contribute to their progression and mutually burden the course of both diseases, which is a necessary prerequisite for effective prevention and treatment of these patients. Materials and methods. A biochemical study of venous blood was carried out in 60 men with gout, aged 30 to 59 years, who were undergoing inpatient treatment in the rheumatology department of Lviv Regional Clinical Hospital. All the examined were men, which is related to the gender-age characteristics of the prevalence of gout. 2 observation groups were formed: the main group consisted of 30 patients with generalized periodontitis on the background of gout; the comparison group included 30 people with generalized periodontitis, not burdened by rheumatological pathology. The results were compared with the indicators of 20 conditionally healthy individuals (control group). The research was carried out in the period between attacks of gouty arthritis, two weeks after therapy with non-steroidal anti-inflammatory drugs. In order for the test results to be objective, 24 hours before blood sampling, patients were recommended to exclude fruit and vegetable juices, caffeine, and alcoholic beverages from their diet, as well as to limit physical and mental exertion. Results and discussion. The results of the research presented the following: the patients of the main group had the highest level of the main marker of purine metabolism – uric acid in blood serum; it was 0.62 ± 0.18 mmol/l with a normal reference range of 0.20 - 0.42 mmol/l. In the comparison group, the laboratory indicator of uric acid content in blood serum was 0.38 ± 0.09 mmol/l and was at the upper limit of reference values, but it was by 1.6 times lower than in the main group, p < 0.05. In the control group, the lowest level of uric acid was observed with a digital value of 0.26 ± 0.06 mmol/l, which was by 1.5 times less than in the control group and by 2.4 times less compared to the data of the main group, p < 0.01. The level of urea, a marker of protein metabolism, in patients with generalized periodontitis on the background of gout was 9.21 ± 2.24 mmol/l and was by 1.3 times higher than the similar indicator of persons not burdened by rheumatological pathology (6.89 ± 1.53 mmol/l, p < 0.01) and by 1.9 times higher than in healthy individuals (4.72 ± 1.08 mmol/l, p < 0.01). Conclusion. According to the results of a biochemical study of the blood serum of patients with generalized periodontitis associated with gout, a significant increase in the concentration of uric acid was established, which indicated a violation of purine metabolism in these patients. Also, in patients with periodontal pathology on the background of gout, violations of protein homeostasis were observed, which was indicated by a high level of urea in the blood serum. Such a situation may indicate the presence, both at the systemic level in general and in periodontal tissues, in particular, of deep destructive processes that affect nuclear structures rich in nucleic acids, and the existence of a correlation between hyperuricemia and the destructive-inflammatory process in periodontics. Violations of purine and protein homeostasis contribute to the progression and mutually burden the course of both diseases
The article presents a review and analysis of relevant available literature sources on etiopathogenetic mechanisms of periodontal disease and liver diseases of viral aetiology, and, in particular, hepatitis B and C viruses. Significant prevalence, pronounced polymorphism of clinical hepatic and extrahepatic manifestations, the incidence rate of liver cirrhosis and hepatocellular carcinoma allows us to consider hepatitis of viral aetiology as a medical and social challenge. Multi-vector liver dysfunctions can cause oral presentations in this group of patients, and in particular, in their periodontal tissues. Viral liver damage is associated with significant impairment of the microbiocenosis in gingival sulcus and periodontal pockets. Dysbiotic changes are characterized by an increase in the number of opportunistic pathogens and anaerobic periodontal pathogens. Exacerbation of dysbiosis along with deterioration of oral hygiene occurs as a consequence of reduced local resistance and hyposalivation due to the sialotropic properties of hepatitis C virus. Significant pathogenetic role in the development of periodontal disease is played by disorders of metabolic and synthetic functions of the liver, as well as hormonal imbalance, metabolic disorders, immune-mediated damage, induction of autoimmune mechanisms and cytokine imbalance. The formation of hepatogenic osteopenia and osteoporosis enhances the loss of bone mass of the alveolar processes in the jaws and, accordingly, the resorption of bone tissue with the further progression of more aggressive forms of generalized periodontitis.
Оцінювання впливу стадії фіброзу печінки на клінічний перебіг захворювань пародонта у хворих із хронічним гепатитом С О. М. Слаба, Л. Ю. Мінько, Х. А. Січкоріз, І. О. КіселикЛьвівський національний медичний університет імені Данила Галицького, Україна Мета роботи -оцінити вплив стадії фіброзу печінки на клінічний перебіг захворювань пародонта у хворих із хронічним гепатитом С.Матеріали та методи. У стоматологічне дослідження включили 122 особи, які хворі на хронічний гепатит С в ана мнезі та лікувались у 7 відділенні Львівської обласної інфекційної клінічної лікарні протягом 2013-2015 років. Діагноз захворювань пародонта встановлювали відповідно до класифікації М. Ф. Данилевського (1994). Клінічний стан тка-нин пародонта оцінювали за допомогою папілярномаргінальноальвеолярного індексу (РМА) в модифікації Parma; пародонтального індексу (РІ); ступеня кровоточивості ясенних сосочків (РВІ). Стадію фіброзу встановлювали згідно з даними медичної карти хворого. Значущість різниці між двома та більше відносними показниками розрахована за допомогою тесту Фішера з Metropolis алгоритмом. Вивчення кореляційної залежності між клінічним станом тканин пародонта та стадією фіброзу печінки у хворих на хронічний вірусний гепатит С здійснили за допомогою рангового коефіцієнта кореляції Спірмена.Результати. Найбільший відсоток хворих зі стадією фіброзу печінки F 0 (70,00 ± 15,28 %) зареєстрований в осіб зі здоровим пародонтом, найменший -у хворих на генералізований пародонтит ІІІ ступеня важкості (7,89 ± 4,37 %). Найбільша частота хворих зі стадією фіброзу печінки F 3 (73,68 ± 7,14 %) також спостерігалась в осіб, які страждають на генералізований пародонтит ІІІ ступеня важкості (73,68 ± 7,14 %).Висновки. Важкість ураження тканин пародонта статистично значуще (р < 0,001) залежить від стадії фіброзу печінки у хворих на хронічний гепатит С. Між клінічним станом тканин пародонта та стадією фіброзу печінки у хворих на хронічний гепатит С встановлений прямий кореляційний зв'язок (R = 0,70; р < 0,001).Оценка влияния стадии фиброза печени на клиническое течение заболеваний пародонта у больных с хроническим гепатитом С О. М. Слаба, Л. Ю. Минько, К. А. Сичкориз, И. А. Киселик Цель работы -оценить влияние стадии фиброза печени на клиническое течение заболеваний пародонта у больных с хроническим гепатитом С. Материалы и методы.Обследовано 122 пациента с хроническим гепатитом С (г. Львов). Установление диагноза за-болеваний пародонта проводили в соответствии с классификацией М. Ф. Данилевского (1994). Клиническое состояние пародонта оценивали по папиллярномаргинальноальвеолярному индексу (РМА) в модификации Parma, пародонталь-ному индексу -РI (A. L. Russel, 1956), индексу Muhlemann и Son -степень кровотечения в области десневых сосочков (РВИ). Стадию фиброза устанавливали по данным медицинской карты. Значимость различия между двумя и больше относительными показателями рассчитана с помощью теста Фишера с Metropolis алгоритмом. Изучение корреляцион-ной зависимости между клиническим состоянием тканей пародонта и стадией фиброза печени у больных ви...