The role of cigarette smoking in periodontal disease and treatment outcomes of dental implant therapy.

Tobacco smoking has been implicated in periodontal pathology through various mechanisms, including perturbations of the inflammatory and host responses to putative periodontal pathogens, alterations in the subgingival microbial communities, and a compromised healing potential of the tissues leading to imbalance of tissue homeostasis. This review provides the evidence for the relationship between cigarette smoking and periodontal disease in an attempt to explain possible mechanisms of how tobacco smoking may exert its negative effects on the periodontal tissues via systemic and localized pathways. Early and more recent studies explore cigarette smoking-induced changes in periodontal clinical indices; in subgingival microbial flora by employing traditional detection methods for selected microorganisms, in addition to modern techniques such as deep sequencing and bioinformatics analyses that are able to fully characterize the microbial communities; and in inflammatory and immune responses critically appraising study limitations and differences in study protocol designs.

Evaluation of stemness properties of cells derived from granulation tissue of peri-implantitis lesions.

Objectives: Peri-implantitis (PI) is an inflammatory disease associated with peri-implant bone loss and impaired healing potential. There is limited evidence about the presence of mesenchymal stromal cells (MSCs) and their regenerative properties within the granulation tissue (GT) of infrabony peri-implantitis defects. The aim of the present study was to characterize the cells derived from the GT of infrabony PI lesions (peri-implantitis derived mesenchymal stromal cells-PIMSCs).

Understanding the microbial components of periodontal diseases and periodontal treatment-induced microbiological shifts.

In the mid-1960s the microbial aetiology of periodontal diseases was introduced based on classical experimental gingivitis studies . Since then, numerous studies have addressed the fundamental role that oral microbiota plays in the initiation and progression of periodontal diseases. Recent advances in laboratory identification techniques have contributed to a better understanding of the complexity of the oral microbiome in both health and disease.

Control of dentin/root sensitivity during non-surgical and surgical periodontal treatment.

Aim: To determine the efficacy of a desensitizing regimen compared to a control in preventing the occurrence and/or alleviating dentin/root sensitivity (DRS) following non-surgical (NSPT) and surgical periodontal treatment (SPT).

Methods: Seventy-four chronic-periodontitis patients (CPP) were randomized into a test group (n = 38) using an in-office prophylaxis paste and a toothpaste at home both containing 8% arginine and calcium carbonate (Pro-Argin(™) Technology) or into a control group (n = 36) receiving a fluoride-free prophylaxis paste and a fluoride toothpaste. The examiner applied the assigned paste onto selected teeth for 3 s following NSPT and for 60 s before flap closure.

Modern approaches to non-surgical biofilm management.

The subgingival dental plaque is a microbial biofilm consisting of highly variable bacterial microcolonies embedded within a self-produced matrix of extracellular polymeric substance. In contrast to microorganisms growing in a planktonic state, the inhabitants of a biofilm are effectively protected within this dense structure from host defense mechanisms and from therapeutic agents, including antimicrobials. The mechanical removal of the microbial biofilm and the establishment of meticulous plaque control measures comprise the key elements for the success of non-surgical periodontal treatment.