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Cigarette smoking represents a major preventable cause of human disease. Smokers have significantly elevated risks of all-cause mortality and developing a variety of pathological conditions. A direct causal relationship between smoking exposure and the prevalence and the severity of periodontal disease has been firmly established. Although the direct cause for periodontitis is oral bacterial infection, smoking is arguably the strongest behavioral risk factor for the incidence and progression of periodontitis. Smoking has a deleterious effect on all the aspects of periodontium. Smokers have been shown to respond less well to nonsurgical as well as surgical therapy than nonsmokers. Based on this evidence, dental health professionals should advise patients about tobacco's negative health effects as well as the benefits of quitting tobacco use, and tobacco cessation counseling should be a part of the armamentarium of the dental office. [ABSTRACT FROM AUTHOR]

Background: Peri-implantitis is a chronic inflammation, resulting in loss of supporting bone around implants. Chronic periodontitis is a risk indicator for implant failure. Both diseases have a common etiology regarding inflammatory destructive response. BRINP3 gene is associated with aggressive periodontitis. However, is still unclear if chronic periodontitis and peri-implantitis have the same genetic background. The aim of this work was to investigate the association between BRINP3 genetic variation (rs1342913 and rs1935881) and expression and susceptibility to both diseases. Methods: Periodontal and peri-implant examinations were performed in 215 subjects, divided into: healthy (without chronic periodontitis and peri-implantitis, n = 93); diseased (with chronic periodontitis and peri-implantitis, n = 52); chronic periodontitis only (n = 36), and peri-implantitis only (n = 34). A replication sample of 92 subjects who lost implants and 185 subjects successfully treated with implants were tested. DNA was extracted from buccal cells. Two genetic markers of BRINP3 (rs1342913 and rs1935881) were genotyped using TaqMan chemistry. Chi-square (p < 0.05) compared genotype and allele frequency between groups. A subset of subjects (n = 31) had gingival biopsies harvested. The BRINP3 mRNA levels were studied by CT method (2ΔΔCT). Mann--Whitney test correlated the levels of BRINP3 in each group (p < 0.05). Results: Statistically significant association between BRINP3 rs1342913 and peri-implantitis was found in both studied groups (p = 0.04). The levels of BRINP3 mRNA were significantly higher in diseased subjects compared to healthy individuals (p = 0.01). Conclusion: This study provides evidence that the BRINP3 polymorphic variant rs1342913 and low level of BRINP3 expression are associated with peri-implantitis, independently from the presence of chronic periodontitis. [ABSTRACT FROM AUTHOR]

Peri-implant diseases are inflammatory lesions which may affect the peri-implant mucosa only (peri-implant mucositis) or also result in loss of supporting bone (peri-implantitis). Peri-implantitis may lead to loss of the implant. Diagnosis of peri-implant disease requires the use of conventional probing to identify the presence of bleeding on probing, and suppuration, both signs of clinical inflammation. Radiographs are required to detect loss of supporting bone. Baseline probing measurements and radiographs should be obtained once the restoration of the implant is completed to allow longitudinal monitoring of peri-implant conditions. Two cross-sectional reports from Sweden indicate that the prevalence of peri-implant disease is high. Smokers and patients who have a history of periodontitis are more at risk for peri-implant disease. The main goal of treatment of peri-implant disease is to control the infection and to prevent disease progression. A number of studies have documented the successful treatment of peri-implant mucositis combining mechanical debridement and chemical plaque control. There is evidence supporting antimicrobial treatment regimens in combination with non-surgical or surgical debridement for peri-implantitis treatment. Long-term data to support these treatment protocols is limited. Whilst it is possible to treat peri-implantitis, prevention is the goal of supportive therapy. [ABSTRACT FROM AUTHOR]