Unstable atherosclerotic plaque is a dangerous clinical condition, possibly leading to acute coronary deficiency resulting in cardiac infarction. Questions about the role of inflammatory factors in the formation of pathological lesions in the endothelium of coronary vessels have often been raised. This condition may be caused by bacteria that are able to initiate clot formation in a blood vessel, destabilizing an atherosclerotic plaque that is already present. The sources of these pathogens are chronic inflammatory processes occurring in the host, including periodontal disease, which is one of the most frequent conditions. The aim of this study was to evaluate the incidence of selected anaerobic bacteria in subgingival and atherosclerotic plaque in patients treated surgically because of coronary vessel obliteration. The study was performed on 20 individuals with chronic periodontitis. Subgingival plaque was collected from periodontal pockets >5 mm. DNA testing was used to identify eight pathogens responsible for periodontal tissue destruction. Material from atherosclerotic plaques was collected from the same patients during bypass surgery, and DNA testing by the same method was performed. In 13 of 20 patients, the pathogens most frequently found in severe chronic periodontitis were also found in coronary vessels. In 10 cases, those species of bacteria were also present in atherosclerotic plaque. The most frequently identified bacteria were Porphyromonas gingivalis and Treponema denticola. In patients with the severe form of chronic periodontitis, it seems that clinical attachment loss is not associated with bacterial permeability into coronary vessels. What is important is the presence of an active inflammatory process expressed by a significantly higher bleeding index in those patients in whom the examined bacterial species were found in atherosclerotic plaque.

This paper presents the current knowledge concerning the role of polymorphisms of IL1A and IL1B genes in periodontitis. Attention has been paid to the role of IL-1 in the pathogenesis of the disease, and to the significance of a genetic test, investigating the presence of composite two polymorphisms of IL-1 gene, as a risk factor for severe periodontitis. The significance of this test for prevention of periodontitis and its therapy has been discussed. IL-1 polymorphisms have been presented and described according to the reference single nucleotide polymorphism (SNP) identification number (rsID), established to eradicate the redundancy of reported polymorphisms in the SNP database processed by the National Center for Biotechnology Information. The prevalence of these genotypes in different populations and ethnic groups and its effect on periodontal health have been discussed. The presented data show inconsistent results. It seems that at least two polymorphisms, rs1800587 and rs1143634, are associated with periodontal inflammation. Therefore, they can be regarded as candidate genes involved in further periodontitis risk assessment. It seems that geographical and ethnical factors can play a great role, as the prevalence of specific polymorphisms varies greatly depending on the population studied.

The uniqueness of periodontal diseases is caused by several factors. This group of diseases is caused by numerous bacterial species formed in the dental biofilm, and one cannot distinguish the specific pathogen that is responsible for the disease initiation or progress (though Gram-negative anaerobic rods are associated with the advanced form of the disease). The disease is both infectious and inflammatory in its nature, and in the state of health there is always a subclinical level of inflammatory response, caused by the so-called harmless bacteria. Negligence in oral hygiene may result in maturation of the biofilm and trigger host response, manifesting clinically as gingivitis or—later and in susceptible subjects—as periodontitis. The article presents the contemporary knowledge of the inflammatory reaction occurring in tissues surrounding the tooth during periodontal inflammation. The most important mechanisms are described, together with implications for clinicists.

Dental implants are, nowadays, established surgical devices for the restoration of lost teeth. Considered as an alternative for traditional prosthetic appliances, dental implants surpass them in reliability and patient feedback. Local drug delivery around the implants promotes osseointegration and reduces peri-implantitis. However, there are currently no methods of a multiple, precise topical administration of drugs to the implant area. Engineering coatings on the implants, drug application on carriers during implantation, or gingival pockets do not meet all requirements of dental surgeons. Therefore, there is a need to create porous implants and other medical devices that will allow a multiple drug delivery at a controlled dose and release profile without traumatic treatment. Due to the growing demand for the use of biologically active agents to support dental implant treatment at its various stages (implant placement, long-term use of dental superstructures, treatment of the peri-implant conditions) and due to the proven effectiveness of the topical application of pharmacological biologically active agents to the implant area, the authors would like to present a review and show the methods and devices that can be used by clinicians for local drug administration to facilitate dental implant treatment. Our review concludes that there is a need for research in the field of inventions such as new medical devices or implants with gradient solid–porous structures. These devices, in the future, will enable to perform repeatable, controllable, atraumatic, and repeatable injections of active factors that may affect the improvement of osteointegration and the longer survival of implants, as well as the treatment of peri-implantitis.

This systematic review analyzes the effects of smoking cessation on oral health outcomes in individuals with type 2 diabetes. The review followed PRISMA guidelines, and the protocol was registered on PROSPERO (CRD42024604271). Risk of bias was assessed using the Joanna Briggs Institute's critical appraisal tools. PubMed, Scopus, and Web of Science were searched on November 7, 2024, alongside references from highly cited journals and conference proceedings. No language or date restrictions were applied. Inclusion criteria were human clinical studies (randomized controlled trials, cohort, case-control, or cross-sectional studies) involving patients with type 2 diabetes, stratified by smoking status (former, current, never smokers), assessing oral health outcomes (e.g., periodontal disease, caries). Studies without detailed smoking status data were excluded. The search retrieved 549 studies, of which 4 (N = 926 participants) met the inclusion criteria. These studies examined smoking status in relation to periodontitis progression and response to periodontal therapy. Overall, the effects smoking cessation in improving periodontal outcomes in this population appears limited. However, methodological limitations were identified, and the studies may have been underpowered for the smoking status subgroup. Evidence on the impact of smoking cessation on oral health in patients with type 2 diabetes remains inconclusive, as large prospective studies specifically designed for this purpose are lacking. While smoking cessation benefits oral health in the general population, its effects on oral outcomes in patients with diabetes remain unclear. Further research is needed to elucidate its impact on patients with type 2 diabetes. A multidisciplinary approach to managing diabetic patients is essential, where dentists not only address oral health but also support healthy behaviors, including smoking cessation, to improve overall diabetes-related complications.