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Plaque Biofilm (plaque + biofilm)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Pro-inflammatory biomarkers during experimental gingivitis in patients with type 1 diabetes mellitus: a proof-of-concept study

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2010
Giovanni E. Salvi
Abstract Aim: To compare gingival crevicular fluid (GCF) biomarker levels and microbial distribution in plaque biofilm (SP) samples for subjects with type 1 diabetes (T1DM) versus healthy subjects without diabetes during experimental gingivitis (EG). Materials and Methods: A total of nine T1DM patients and nine healthy controls of age and gender similar to the T1DM patients were monitored for 35 days during EG. Hygiene practices were stopped for 3 weeks, and GCF, SP, plaque index (PI) and gingival index were determined. IL-1,, IL-8, MMP-8 and MMP-9 were quantified by enzyme-linked immunosorbent assay, and SP samples were assessed by DNA,DNA hybridization for a panel of 40 subgingival microbial species. Results: IL-1, levels in T1DM patients were elevated compared with healthy individuals, and showed differences between groups at 7,21 days while healthy patients showed IL-1, increases from baseline to 14,21 days (p<0.05). Differences were observed in MMP-9 levels between patients with and without T1DM at 7,14 days (p<0.05). Orange complex species and PI measurements displayed a superior correlation with biomarker levels when compared with other complexes or clinical measurements during EG. Conclusions: The mean GCF biomarker levels for IL-1, and MMP-8 were most significantly elevated in T1DM subjects compared with healthy individuals during EG, not resulting from differences in the mean PI or microbial composition. [source]

Recent concepts in plaque formation

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 2003
J.-P. Bernimoulin
Abstract Dental plaque is an adherent, bacterial film, and is the main pathological agent for periodontal diseases. The formation of dental plaque can occur both supragingivally and subgingivally. The development of plaque is a three-step process. Following the formation of a pellicle, pioneer micro-organisms will adhere to it, proliferate and form colonies. The final stage involves the aggregation of filamentous organisms and spirochetes into a cohesive biofilm. Many products of the plaque bacteria reach the subepithelial tissue, causing inflammatory responses such as increased vascularity and leukocyte diapedesis. Both supragingival and subgingival plaque may form a hard, mineralized mass called calculus. The surface of calculus harbours bacteria, which may exacerbate the inflammatory responses. An effective oral antiseptic must be active against a wide range of Gram-positive and Gram-negative bacterial species, including streptococci and fusobacteria. Ideally, an effective agent would also penetrate the plaque biofilm. Data show that essential oil and chlorhexidine mouthwashes have the broadest antimicrobial effects. [source]

Non-oral bifidobacteria and the aciduric microbiota of the denture plaque biofilm

MOLECULAR ORAL MICROBIOLOGY, Issue 3 2010
M. Mantzourani
Summary The microbiota of the denture plaque biofilm colonizing the fitting surface of dentures in edentulous subjects with healthy palates (n = 20) and in edentulous subjects with denture stomatitis (n = 20) was studied. The numbers of bacteria colonizing the dentures of healthy subjects was significantly less than the numbers colonizing the dentures of stomatitis subjects. The proportions and frequency of isolation of mutans streptococci, lactobacilli, bifidobacteria and yeasts were significantly (P < 0.05) greater in the subjects with denture stomatitis. The proportions of these organisms in the denture plaque biofilm of the subjects with denture stomatitis were similar to those found in carious lesions, indicating that the site is a low pH environment. The predominant bifidobacterial species in the mouths of dentate subjects is Bifidobacterium dentium but in the edentulous subjects wearing dentures B. dentium was isolated from only one of the 20 subjects with denture stomatitis and from none of the 20 subjects with healthy palates. Instead, Bifidobacterium breve, Bifidobacterium scardovii and Bifidobacterium longum subsp. longum were isolated. Only a single non-oral bifidobacterial species was isolated from each individual and repetitive extragenic palindromic- and BOX-polymerase chain reaction typing methods indicated that the same genotypes were shared between subjects. Using deferred antagonism spot plate assays, interspecies inhibition was demonstrated between oral isolates of B. dentium, B. breve, B. scardovii and B. longum subsp. longum. Here we have shown that bifidobacteria and caries-associated microbiota are present in denture plaque at levels similar to those of carious lesions and B. dentium cannot be maintained in an edentulous mouth. [source]

The immunopathogenesis of periodontal disease

AUSTRALIAN DENTAL JOURNAL, Issue 2009
EJ Ohlrich
Abstract Treatment planning in periodontics, as with any disease, must be based on an understanding of the aetiology and pathogenesis of the disease. In this context, it has slowly become recognized over the past three decades that while plaque is the cause of the disease, it is the innate susceptibility of the host that determines the ultimate outcome of the disease process. Innate susceptibility, in turn, is determined by the nature of the immune response to the specific periodontopathic complexes comprising the plaque biofilm. The aim of this review was to examine current understanding of the immunopathogenesis of chronic periodontitis with respect to its possible clinical implications in terms of treatment planning and risk assessment. Numerous studies have demonstrated that the periodontitis lesion itself involves predominantly B cells and plasma cells, while the gingivitis lesion is primarily a T cell mediated response. This led to the concept over 30 years ago that the development of periodontitis involves a switch from a T cell lesion to one involving large numbers of B cells and plasma cells. It is also well recognized that control of this shift is mediated by a balance between the so-called Th1 and Th2 subsets of T cells, with chronic periodontitis being mediated by Th2 cells. More recently, T regulatory (Treg) and Th17 cells have been demonstrated in periodontal tissues, raising the possibility that these cells are also important in the immunoregulation of periodontal disease. The clinical implications of these observations can be seen in the fact that identification of Th1/Th2 and Treg/Th17 cytokine gene expression in the peripheral blood and salivary transcriptomes is now being trialled as a possible marker of disease susceptibility. If this proves to be the case, a chairside salivary diagnostic could be developed within the next five to 10 years. [source]