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. Periodontal treatment outcomes and implant therapy outcomes are reviewed in an attempt to shed light on possible mechanisms for the inferior treatment outcome noted in smokers. The potential harmful effects of passive smoking are also reviewed, providing evidence for the advantages of smoking cessation. Quitting cigarette smoking should be recommended by the dentist, and effort should be made to inform smokers about the negative effects of smoking on the periodontal status and implant therapy outcomes.

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). MATERIAL AND METHODS: PIMSC cultures were established from GT harvested from PI lesions with a pocket probing depth ≥6 mm, bleeding on probing/suppuration, and radiographic evidence of an infrabony component from four systemically healthy individuals. Cultures were analyzed for embryonic (SSEA4, NANOG, SOX2, OCT4A), mesenchymal (CD90, CD73, CD105, CD146, STRO1) and hematopoietic (CD34, CD45) stem cell markers using flow cytometry. PIMSC cultures were induced for neurogenic, angiogenic and osteogenic differentiation by respective media. Cultures were analyzed for morphological changes and mineralization potential (Alizarin Red S method). Gene expression of neurogenic (NEFL, NCAM1, TUBB3, ENO2), angiogenic (VEGFR1, VEGFR2, PECAM1) and osteogenic (ALPL, BGLAP, BMP2, RUNX2) markers was determined by quantitative RT-PCR. RESULTS: PIMSC cultures demonstrated high expression of embryonic and mesenchymal stem cell markers with inter-individual variability. After exposure to neurogenic, angiogenic and osteogenic conditions, PIMSCs showed pronounced tri-lineage differentiation potential, as evidenced by their morphology and expression of respective markers. High mineralization potential was observed. CONCLUSIONS: This study provides evidence that MSC-like populations reside within the GT of PI lesions and exhibit a multilineage differentiation potential. Further studies are needed to specify the biological role of these cells in the healing processes of inflamed PI tissues and to provide indications for their potential use in regenerative therapies.

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. Modern culture-independent methods such as human oral microbial identification microarray and next-generation sequencing have been used to identify a wide variety of microbial taxa residing in the gingival sulcus and the periodontal pocket. The first theory of the 'non-specific plaque' hypothesis gave rise to the 'ecological plaque' hypothesis and more recently to the 'polymicrobial synergy and dysbiosis hypothesis'. Periodontitis is now considered to be a multimicrobial inflammatory disease in which the various bacterial species within the dental biofilm are in a dysbiotic state and this imbalance favours the establishment of chronic inflammatory conditions and ultimately the destruction of tooth-supporting tissues. Apart from the known putative periodontal pathogens, the whole biofilm community is now considered to play a role in the establishment of inflammation and the initiation and progression of periodontitis in a susceptible host. Treatment is unlikely to eliminate putative pathogens but, when it is thoroughly performed it has the potential to establish a healthy ecosystem by altering the microbial community in numbers and composition and also contribute to the maturation of the host immune response.

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. Patients brushed with the assigned toothpaste twice daily throughout the study. DRS to air stimulus was assessed by the Schiff scale (0-3) and the Visual Analog Scale (VAS: 0-100 mm) six times over 17 weeks. RESULTS: In the test group, VAS scores significantly decreased at 8, 11 and 17 weeks from baseline (p ≤ 0.003) and Schiff scores at 8 and 11 weeks from baseline (p ≤ 0.014). The control group exhibited significant increases in VAS and Schiff during the study period (p ≤ 0.006). Marked inter-group differences were noted at all time points (p < 0.001). CONCLUSIONS: The combined use of desensitizing products (8% arginine and calcium carbonate) in-office and at-home prevented DRS development and maintained this effect for 17 weeks following NSPT and SPT.

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. Ultrasonic devices are effective in disrupting the biofilm, and carefully remove soft and hard deposits from a root surface with minimal trauma to the tooth structure. Controversies and modern trends in non-surgical periodontal therapy - such as quadrant-wise treatment modalities versus full-mouth approaches, hand-versus power-driven instrumentation, and the time frame of non-surgical periodontal therapy - are discussed here in depth in order to provide an insight into modern approaches to non-surgical biofilm management. Clinical, microbiological and immunological findings following different treatment protocols, in addition to cost-effective benefits of these clinical modalities, are discussed.