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.

As implant treatment has been integrated in contemporary dental practice, complications with the forms of peri-implant mucositis and peri-implantitis have also increased in prevalence. Peri-implantitis is the more severe biological complication and is defined as an inflammatory disease affecting peri-implant tissues resulting in bone and eventually implant loss. In addition, the treatment of peri-implantitis has currently become a substantial global economic burden. In the current study, a search was conducted in several electronic databases using specific keywords relevant to the article’s main topic. An increasing number of scientific reports have investigated the etiopathology of peri-implant diseases, focusing mainly on peri-implantitis. Microbial biofilm consists an important etiological factor of peri-implant pathology analogous to periodontal diseases. Although several data confirm that peri-implant infections are dominated by gram-negative bacteria, similar to periodontal infections, there is evidence that some cases may harbor a distinct microbiota, including opportunistic microorganisms and/or uncultivable species. Additionally, data support that several parameters, such as genetic predisposition of individual patients, occlusal overload, and local factors such as titanium particles and excess cement, may be implicated in peri-implantitis pathogenesis. Simultaneously, the release of titanium metal particles and their biological consequences or the presence of excess cement in the adjacent peri-implant tissues have also been suggested as factors that contribute to peri-implant pathology. A specific line of research also indicates the role of foreign body response to implant installation. This narrative review aims to discuss the current concepts of etiopathogenetic factors implicated in peri-implantitis.

The concept of gingival phenotype and width of keratinized gingiva influencing the diagnosis and treatment in the periodontal scenario is relatively new. Soft and hard tissue dimensions of oral tissues are considered essential parameters in daily clinical practice. Factors such as the biotype category and the width of the keratinized gingiva help dentists seek the perfect therapy plan for each patient to achieve long-term stability of periodontal health. Several methods have been proposed to categorize phenotypes and each phenotype is characterized by various clinical characteristics. This review aims to discuss the possible association between the gingival phenotype and the width of keratinized gingiva along with the results appeared. After a rigorous search in major electronic databases, the results of the included studies indicated that the width of keratinized gingiva seems to be associated with the periodontal phenotype, with thick biotypes being characterized by a more pronounced keratinized gingival width. However, the heterogeneity of the included studies did not allow to make a conclusion about a direct relationship.

Background and Objective Azurocidin is a neutrophil‐derived protein in gingival crevicular fluid (GCF) which, according to relevant studies, might correlate with periodontal disease. The aim of the present study was to evaluate azurocidin as a potential biomarker for chronic periodontitis. Material and Methods One hundred and one patients participated in the study, divided into two groups. Forty‐eight were included in the periodontally healthy group (HP) and fifty‐three in the chronic periodontitis group (CP). Clinical indices included probing depth (PD), recession (REC), clinical attachment level (CAL), bleeding on probing (BOP) and plaque (PL). Pooled GCF samples were collected with paper strips, freezed in liquid nitrogen (−196°C), stored at −80°C, and the levels of azurocidin were analyzed with ELISA. Values were transformed and expressed for comparisons in pg/30 s sample. Statistical comparisons were performed using non‐parametric tests (Mann‐Whitney) at the 0.05 level. Furthermore, the diagnostic accuracy of the procedure was assessed with receiver operator characteristic curves (ROC), areas under the curve (AUC), and the Youden's J Index calculated. Results Demographic data were comparable between the two groups. Clinical parameters and the levels of azurocidin were statistically significantly higher in the CP group when compared to the HP group (Mann‐Whitney test, P < .05). Quantitative data from ELISA demonstrated a high diagnostic accuracy of azurocidin, with AUC calculated higher than 0.9 at the 0.000 level. Conclusion Azurocidin in GCF is a promising biomarker for periodontal disease. The results of the present study agree with previous studies in the literature showing an up‐regulated trend in the levels of azurocidin in periodontitis patients.

Objective: The current cross-sectional study aimed to investigate the prevalence of gingival recession (REC) in a sample of young individuals. In addition, the association with several risk factors was examined.Materials & methods: A 104 subjects, aged 18-30 years old, were randomly enrolled in the study. Participants were requested to fill in a simple structured questionnaire in order to provide information on dental hygiene habits, educational level, smoking and history of orthodontic treatment. Afterwards, all the included individuals were subjected to a thorough clinical periodontal examination including gingival recession (REC), gingival biotype, plaque levels and gingival bleeding index (GBI) assessment. Results:The mean prevalence of REC in the studied population surpassed 50% with an equal distribution among females and males. The most common teeth associated with REC were the lower left canine and left 1st premolar. Among the examined variables, only the bleeding index was found to be associated with the presence of REC.Conclusions: Gingival recession was a prevalent condition among young individuals.Gingival inflammation was found to be the most significant factor affecting the incidence of REC.