Both techniques were effective for maxillary sinus augmentation, and after 6 months of healing, the addition of L-PRF in DBBM did not improve the amount of regenerated bone or the amount of the graft integrated into the newly formed bone under histological and histomorphometric evaluation.
Good overall stability and a small tooth loss rate were observed in this cohort of chronic periodontitis cases under SPT in private practice. Patient-based and tooth-based prognosis systems may be used to estimate the risk of tooth loss.
Periodontal diseases are common chronic inflammatory diseases caused by pathogenic microorganisms colonising the subgingival area and inducing local and systemic elevations of pro-inflammatory cytokines resulting in tissue destruction. Apparition and evolution of periodontal diseases are influenced by many local or systemic risk factors. Psychological stress has been suggested as one of them and may negatively influence the outcome of periodontal treatment. However, mechanisms explaining the possible relationship between stress and increased susceptibility to periodontal disease remain poorly understood. Several stress markers are found in blood and saliva of patients with periodontal diseases and influence the development of periodontal diseases by several mechanisms including modifications of the inflammatory response and changes in the composition of the dental biofilm. The aim of this review is to provide an insight into the relationship between psychological stress and periodontal diseases.
Dental calculus represents the first fossilized record of bacterial communities as a testimony of evolutionary biology. The development of dental calculus is a dynamic process that starts with a nonmineralized biofilm which eventually calcifies. Nonmineralized dental biofilm entraps particles from the oral cavity, including large amounts of oral bacteria, human proteins, viruses and food remnants, and preserves their DNA. The process of mineralization involves metabolic activities of the bacterial colonies and strengthens the attachment of nonmineralized biofilms to the tooth surface. From a clinical point of view, dental calculus always harbors a living, nonmineralized biofilm, jeopardizing the integrity of the dento-gingival or implanto-mucosal unit. This narrative review presents a brief historical overview of dental calculus formation and its clinical relevance in modern periodontal practice.
Polycystic ovary syndrome (PCOS) is a hormonal disorder of women that not only is the leading cause of infertility but also shows a reciprocal link with oral health. This study aimed to investigate the hypothesis that the levels of putative periodontal pathogens in saliva and their antibody response in serum are elevated in PCOS, compared to systemic health. A total of 125 women were included in four groups; 45 women with PCOS and healthy periodontium, 35 women with PCOS and gingivitis, 25 systemically and periodontally healthy women, 20 systemically healthy women with gingivitis. Salivary levels of seven putative periodontal pathogens were analyzed by quantitative real-time polymerase chain reaction and serum antibody levels were analyzed by ELISA. In women with PCOS, salivary Porphyromonas gingivalis, Fusobacterium nucleatum, Streptococcus oralis and Tannerella forsythia levels were higher than matched systemically healthy women, particularly in the case of gingivitis. Aggregatibacter actinomycetemcomitans and Treponema denticola levels were similar among study groups. The presence of PCOS also enhanced P. gingivalis, Prevotella intermedia and S. oralis serum antibody levels, when gingivitis was also present. Gingival inflammation correlated positively with levels of the studied taxa in saliva, particularly in PCOS. The presence of P. gingivalis and F. nucleatum in saliva also exhibited a strong positive correlation with the corresponding serum antibody levels. In conclusion, as an underlying systemic endocrine condition, PCOS may quantitatively affect the composition of oral microbiota and the raised systemic response to selective members of this microbial community, exerting a confounding role in resultant gingival inflammation and periodontal health. The most consistent effect appeared to be exerted on P. gingivalis.
OBJECTIVES: To test whether or not vascularized interpositional periosteal-connective tissue grafts are as successful as free subepithelial connective tissue grafts in augmenting volume defects in the anterior maxilla. MATERIAL AND METHODS: Twenty subjects with Seibert class 1 ridge defects in the anterior maxilla were randomly, equally assigned to augmentation by vascularized interpositional periosteal-connective tissue graft (test) or free subepithelial connective tissue graft (control). Clinical periodontal parameters at teeth adjacent to the gap were recorded, and conventional impressions were taken prior to surgery (baseline = t0 ) and 1 (t1 ), 3 (t3 ) and 6 (t6 ) months after surgery. The casts were optically scanned, digitized and analyzed for ridge contour changes in the augmented area. Data were subjected to nonparametric statistics. RESULTS: The contour changes in labial distance between baseline and follow-up for the control group were (median, range) 1 mm, 0.37-1.45 (t0 -t1 ); 1.18 mm, 0.39-1.40 (t0 -t3 ); and 0.63 mm, 0.28-1.22 (t0 -t6 ) and for test group 1.21 mm, 0.74-2.47 (t0 -t1 ); 1.26 mm, 0.50-1.71 (t0 -t3 ); and 1.18 mm, 0.16-1.75 (t0 -t6 ). Significantly less shrinkage of the graft was observed in the test group after 6 months (P = 0.03). Clinical periodontal parameters at the neighboring teeth were stable over the follow-up period and did not differ between groups. CONCLUSIONS: Augmentation of single tooth gaps with moderate ridge defects in the anterior maxilla was successfully performed using both techniques. However, after 6 months, sites treated by the pediculated graft were superior in maintaining the initially augmented volume and showed less shrinkage of the graft. This could be attributed to better perfusion of the pediculated graft. Abstract:Objectives: To test whether or not vascularized interpositional periosteal-connective tissue grafts are as successful as free subepithelial connective tissue grafts in augmenting volume defects in the anterior maxilla.Material and Methods: 20 subjects with Seibert class 1 ridge defects in the anterior maxilla were randomly, equally assigned to augmentation by vascularized interpositional periostealconnective tissue graft (test) or free subepithelial connective tissue graft (control). Clinical periodontal parameters at teeth adjacent to the gap were recorded and conventional impressions were taken prior to surgery (baseline=t0) and 1 (t1), 3 (t3) and 6 (t6) months after surgery. The casts were optically scanned, digitized and analyzed for ridge contour changes in the augmented area. Data were subjected to non-parametric statistics.Results: The contour changes in labial distance between baseline and follow-up for the control group were (median; range) 1mm; 0.37-1.45 (t0-t1), 1.18mm; 0.39-1.40 (t0-t3) and 0.63mm; 0.28-1.22 (t0-t6) and for test group 1.21mm; 0.74-2.47 (t0-t1), 1.26mm; 0.50-1.71 (t0-t3) and 1.18mm; 0.16-1.75 (t0-t6). Significantly less shrinkage of the graft was observed in the test group after 6 months (p=0.03). Clinical...
At present, there is insufficient evidence to answer the question on the differences in clinical outcome in terms of CBL between implants placed in sites with initial soft tissue thickness <2 mm and those with ≥2 mm. Further, well-designed controlled clinical studies are needed to analyze the effect of soft tissue thickness on the clinical outcomes of dental implants.
Aim Gestational diabetes mellitus (GDM), gingivitis, infection with specific periodontal pathogens and systemic inflammation each increase the risk for poor pregnancy outcome. We set out to monitor the interactions of gingivitis and GDM with respect to oral infection and the systemic inflammatory burden. Materials and Methods Four case–control groups (n = 117) were recruited, (1) No gingivitis, No GDM (n = 27); (2) Gingivitis, No GDM (n = 31); (3) No gingivitis, GDM (n = 21); and (4) Gingivitis, GDM (n = 38). Oral infection with three key periodontal pathogens was determined by PCR. Systemic inflammation was determined by quantification of CRP by EIA. Results Gingivitis during pregnancy was associated with oral infection with Porphyromonas gingivalis, Filifactor alocis and Treponema denticola and combinations thereof (all p < 0.01). GDM was also associated with increased infection with individual and multiple oral pathogens (all p < 0.05). Gingivitis during pregnancy led to a 325% increase in systemic CRP (mean, 2495 versus 8116 ng/ml, p < 0.01). Conclusions Diabetes and gingivitis act in concert to increase risk biomarkers for poor pregnancy outcome.
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