ABSTRACT
Periodontitis is a complex polymicrobial disease of the oral cavity that affects tooth-supporting tissues. It is caused by multiple factors, such as pathogenic bacteria, genetic predisposition, and host immune response factors. The pathogenesis of periodontal disease involves the complex interrelations among bacterial toxins, several populations of cells, and host cell-secreted inflammatory mediators. Generally, periodontitis is characterized by the formation of intricate and varied biofilms of microbes on the tooth surface, commonly known as dental plaque. Activation of defense cells is characterized by releasing inflammatory mediators, such as proteases, acidic metabolites, cytokines, interleukins, and chemokines, which destroy tissue and ultimately cause bone resorption. The individual periodontal condition has a significant impact on systemic homeostasis, and its disruption can cause the development of some metabolic disorders. This review article summarizes the latest studies on the pathogenesis of periodontitis and describes the role of inflammatory mediators and genetic polymorphism in individuals, as well as relationships with some metabolic conditions. The information is collected from PubMed, Scopus, ScienceDirect, SpringerLink, and clinicaltrials.gov.
ABSTRACT
Dental implants to replace lost teeth are a common dentistry practice nowadays. Titanium dental implants display a high success rate and improved safety profile. Nevertheless, there is an increasing peri-implantitis (PI), an inflammatory disease associated with polymicrobial infection that adversely affects the hard and soft tissues around the implant. The present review highlights the contribution of different metabolic conditions to PI. The considerations of both local and systemic metabolic conditions are crucial for planning successful dental implant procedures and during the treatment course of PI. Un- or undertreated PI can lead to permanent jaw bone suffering and dental implant losses. The common mediators of PI are inflammation and oxidative stress, which are also the key mediators of most systemic metabolic disorders. Chronic periodontitis, low-grade tissue inflammation, and increased oxidative stress raise the incidence of PI and the underlying systemic metabolic conditions, such as obesity, diabetes mellitus, or harmful lifestyle factors (cigarette smoking, etc.). Using dental biomaterials with antimicrobial effects could partly solve the problem of pathogenic microbial contamination and local inflammation. With local dentistry considering factors, including oral microbiota and implant quality control, the inclusion of the underlying systemic metabolic conditions into the pre-procedure planning and during the treatment course should improve the chances of successful outcomes.
ABSTRACT
OBJECTIVE: Introduction: Taking into account the patho-immune mechanisms of formation of inflammatory process in periodontium, there is a necessity for in-depth study of the pathogenesis of periodontal diseases from the position of changes in the reactivity of the organism. The aim: Carrying out a comparative estimation of phagocytic activity of leukocytes of animals with inflammation in periodontium with altered reactivity. PATIENTS AND METHODS: Materials and methods: Experiments were performed on 30 white rats: Group I - 10 white rats with hypoergic reaction; Group ÐÐ - 10 white rats with hyperergic reaction; Group III - 10 white rats with normergic reaction - control group. Slaughter and blood sampling under thiopental anesthesia was performed 7 days after the beginning of the experiment. The percentage of phagocytic leukocytes - phagocytic index, phagocytic number were determined and the index of phagocytic activity was calculated. RESULTS: Results: The phagocytic index (Fi,%) decreased by 2,09 times (p <0,05) at hypoergic, it increased by 1,37 times (p <0,05) at hyperergic; the index of phagocytic activity (IFA) decreased by 1.96 times at hypoergic (p <0.05); growth was 1.94 times (p <0.05) in the hyperergic group of animals. In both experimental groups, the phagocyte number (Fu) increased by 6.25% and 41.7%, with hypoergic and hyperergic, respectively. CONCLUSION: Conclusions: Different directions of changes of the phagocytic activity were observed: increase of these parameters at hyperergic and decrease at hypoergic. An increase in phagocyte number was likely to indicate some autonomy of the process of phagocytosis and independence from the reactivity of the organism.
