The prevalence of obesity has increased substantially over the past decades in most industrialized countries. Obesity is a systemic disease that predisposes to a variety of co-morbidities and complications that affect overall health. Cross-sectional studies suggest that obesity is also associated with oral diseases, particularly periodontal disease, and prospective studies suggest that periodontitis may be related to cardiovascular disease. The possible causal relationship between obesity and periodontitis and potential underlying biological mechanisms remain to be established; however, the adipose tissue actively secretes a variety of cytokines and hormones that are involved in inflammatory processes, pointing toward similar pathways involved in the pathophysiology of obesity, periodontitis, and related inflammatory diseases. We provide an overview of the definition and assessment of obesity and of related chronic diseases and complications that may be important in the periodontist's office. Studies that have examined the association between obesity and periodontitis are reviewed, and adipose-tissue-derived hormones and cytokines that are involved in inflammatory processes and their relationship to periodontitis are discussed. Our aim is to raise the periodontist's awareness when treating obese individuals.
Subjects with RA have significantly increased periodontal attachment loss compared to controls. Oral hygiene may only partially account for this association.
After increasing the width of the attached gingiva by free palatal mucosa transplants, 20 procedures with coronal flap repositioning were performed on 41 teeth with gingival recessions in 13 young adults. The amount of gingival recession and the clinical gingival sulcus depth were measured pre-operatively and 1, 6 and 12 months after surgery; the amount of osseous dehiscence was measured during surgery. No significant differences were found among reduction values of gingival recession by reattachment 1, 6 and 12 months post-operatively. Although a significant correlation was found between the degree of gingival recession preoperatively and 1 month post-operatively, non was found between the amount of alveolar bone dehiscence and gingival recession 1 month post-operatively.
As the additional use of Emdogain together with coronally advanced flap technique for recession coverage showed no difference in the overall clinical outcome, there is no clear benefit to combine Emdogain with this surgical technique.
Periodontitis is one of the most common chronic inflammatory diseases. A number of putative bacterial pathogens have been associated with the disease and are used as diagnostic markers. In the present study, we compared the prevalence of oral bacterial species in the subgingival biofilm of generalized aggressive periodontitis (GAP) (n ؍ 44) and chronic periodontitis (CP) (n ؍ 46) patients with that of a periodontitis-resistant control group (PR) (n ؍ 21). The control group consisted of subjects at least 65 years of age with only minimal or no periodontitis and no history of periodontal treatment. A total of 555 samples from 111 subjects were included in this study. The samples were analyzed by PCR of 16S rRNA gene fragments and subsequent dot blot hybridization using oligonucleotide probes specific for Aggregatibacter (Actinobacillus) actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, a Treponema denticola-like phylogroup (Treponema phylogroup II), Treponema lecithinolyticum, Campylobacter rectus, Fusobacterium spp., and Fusobacterium nucleatum, as well as Capnocytophaga ochracea. Our data confirm a high prevalence of the putative periodontal pathogens P. gingivalis, P. intermedia, and T. forsythia in the periodontitis groups. However, these species were also frequently detected in the PR group. For most of the species tested, the prevalence was more associated with increased probing depth than with the subject group. T. lecithinolyticum was the only periodontopathogenic species showing significant differences both between GAP and CP patients and between GAP patients and PR subjects. C. ochracea was associated with the PR subjects, regardless of the probing depth. These results indicate that T. lecithinolyticum may be a diagnostic marker for GAP and C. ochracea for periodontal health. They also suggest that current presumptions of the association of specific bacteria with periodontal health and disease require further evaluation.
Successful bone augmentation requires predictable space maintenance and adequate exclusion of those cells that lack osteogenetic potential from the defect area. Natural bone mineral is considered to be osteoconductive and is used as space maker in combination with membrane barrier techniques. The aim of this study was to compare qualitative histological results achieved by using deproteinized bovine bone mineral (DBBM) as a space maintainer and a new collagen barrier (Ossix, test group) vs. the same bone substitute and the standard e-PTFE membrane (Gore-Tex), control group). Twenty-eight patients were randomly assigned to the test or the control group. Seven months after augmentation procedures, biopsies were obtained at reentry and were analysed histomorphometrically. In all, 14 specimens of group I (test group, Ossix) and 13 specimens of group II (controls, PTFE-membranes) showed close qualitative similarity of their histologies. Histomorphometrically, total mineralized bone area was 42% +/- 18% in group I vs. 39% +/- 15% in group II. The unmineralized tissue area was 44% +/- 15% vs. 46% +/- 12% and the area of DBBM remnants 14% +/- 9% and 15% +/- 12%, respectively. The differences were statistically nonsignificant (Mann-Whitney test). The occurrence of barrier exposure did not interfere with the histological outcome either in the test or in the control group. The new collagen barrier combined with the DBBM provided qualitative bone regeneration comparable to the standard e-PTFE material combined with the same mineral.
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