Некоторые аспекты патогенеза патологии пародонта при хронической болезни почек
- № 4(65) 2016
Страницы:
99
–
104
Язык: русский
Аннотация
Взаимосвязь между общесоматическими патологиями и состоянием органов полости рта обусловлена нарушениями метаболизма, гемодинамики, микроциркуляции, иммунологическими и нейрорегуляторными изменениями. Иммунологические сдвиги при генерализованном пародонтите характеризуются нарушениями во взаимодействии факторов неспецифической резистентности организма, угнетением клеточного и гуморального иммунитета, а также
подавлением относительно автономной системы местного иммунитета с дисбалансом показателей цитокинов.
Имеет место морфологическая и иммунологическая сопряженность патологических процессов в тканях почек и пародонта у больных хронической болезнью почек, которые проявляются лимфоцитарной инфильтрацией,
фиброзом, поражением сосудов микроциркуляторного русла. Почечная заместительная терапия может влиять на
состояние пародонтальных тканей, включая гингивальную гиперплазию при иммуносупрессии после трансплантации
почки, увеличение микробной контаминации, воспаление десен, отложение зубных камней и возможное увеличение распространенности и тяжести деструктивных процессов пародонта. Кроме того, недиагностированный пародонтит может оказывать существенно влиять на результаты терапии пациентов с ХБП в терминальной стадии.
The relationship between somatic pathology and the state of the oral cavity caused by impaired metabolism, hemodynamics, microcirculation, immunological and neuro regulatory changes. Immunological changes in generalized parodontitis are characterized by disturbances in the interaction of factors of nonspecific resistance of the organism, inhibition of cellular and humoral immunity, as well as the suppression of relatively autonomous system of local immunity with an imbalance indicators cytokines. There is a morphological and immunological conjugate of pathological processes in the tissues of the kidneys and parodontal patients with chronic kidney disease who manifest lymphocytic infiltration, fibrosis, vascular lesions of the microvasculature. It is found that the levels of IL-6 and IL-8 in saliva significantly correlated with the development of diseases of the oral mucosa in patients with chronic kidney disease. Renal replacement therapy may affect the state of parodontal tissues, including gingival hyperplasia with immunosuppression after kidney transplantation, an increase of microbial contamination, gingivitis, tartar, and a possible increase in the prevalence and severity of periodontal destructive processes. Furthermore, undiagnosed parodontitis may have a significant aggravating effects on the treatment of patients with CKD in the terminal stage.
The relationship between somatic pathology and the state of the oral cavity caused by impaired metabolism, hemodynamics, microcirculation, immunological and neuro regulatory changes. Immunological changes in generalized parodontitis are characterized by disturbances in the interaction of factors of nonspecific resistance of the organism, inhibition of cellular and humoral immunity, as well as the suppression of relatively autonomous system of local immunity with an imbalance indicators cytokines. There is a morphological and immunological conjugate of pathological processes in the tissues of the kidneys and parodontal patients with chronic kidney disease who manifest lymphocytic infiltration, fibrosis, vascular lesions of the microvasculature. It is found that the levels of IL-6 and IL-8 in saliva significantly correlated with the development of diseases of the oral mucosa in patients with chronic kidney disease. Renal replacement therapy may affect the state of parodontal tissues, including gingival hyperplasia with immunosuppression after kidney transplantation, an increase of microbial contamination, gingivitis, tartar, and a possible increase in the prevalence and severity of periodontal destructive processes. Furthermore, undiagnosed parodontitis may have a significant aggravating effects on the treatment of patients with CKD in the terminal stage.