TL;DR: It was found that mild gingivitis could be diagnosed clinically at approximately the same time as the complex flora was established and sub-clinical inflammation started much earlier, probably as a reaction to the first phases of plaque development.
Abstract: After 9–21 days without oral hygiene eleven experimental subjects with previously excellent oral hygiene and healthy gingivae developed heavy accumulations of plaque and generalized mild gingivitis. The individual rate of development of gingivitis was closely correlated with the rate of plaque accumulation. Characteristic bacteriological changes were revealed in the plaque along the gingival margin during this experiment. Initially, i.e. when the teeth were clean and the gingiva healthy, the extremely sparse plaque flora consisted almost exclusively of gram-positive cocci and rods. The first phase of plaque development occurred during the first 2 days without oral hygiene and consisted of a proliferation of the gram-positive cocci and rods and an addition of about 30 per cent gram-negative cocci and rods. During the second phase (after 1–4 days) fusobacteria and filaments appeared and increased until they each made up about seven per cent of the flora. During the third phase (after 4–9 days) the flora was supplemented with spirilla and spirochetes, and at the end of the period without oral hygiene each of these two groups of organisms accounted for about two per cent of the plaque flora. In specific areas the gingival condition was correlated with the composition of the plaque and it was found that mild gingivitis could be diagnosed clinically at approximately the same time as the complex flora was established. However, sub-clinical inflammation started much earlier, probably as a reaction to the first phases of plaque development. When oral hygiene was reinstituted, the plaque in most areas disappeared in 1–2 days and after 7–11 days the Plaque Index for each subject was as low as before the experiment. Correspondingly, after 1–2 days most tooth surfaces only harbored the original sparse flora of gram-positive cocci and rods. The gingival inflammation in an area usually disappeared one day after the plaque had been removed.
TL;DR: Results support the assertion that B. forsythus is associated with advancedperiodontitis as well as recurrent periodontitis, and monitoring the subgingival proportions of B.forsythus may be of diagnostic value in patients on maintenance therapy.
Abstract: Bacteroides forsythus, a newly named species from the human mouth, possesses a distinct cell wall ultrastructure and a unique set of cell surface antigens. To determine the distribution of B. forsythus in the periodontal region, supragingival plaque was collected from 16 healthy adults and from 11 adults with mild gingivitis, 12 with severe gingivitis and 17 with periodontitis. Subgingival samples from 27 diseased sites were examined as well. B. forsythus was located in plaque smears by indirect immunofluorescence microscopy. Rabbit antibody to B. forsythus strain FDC 335 constituted the primary antibody and fluoresceinlabelled goat-antirabbit antibody the secondary antibody. There was a significant difference (p<0.05) between the proportions of B. forsythus in supragingival samples of healthy subjects (0.2%) vs. individuals with mild gingivitis (1.3%), severe gingivitis (1.0%) and adult periodontitis (0.9%). A significant difference (p< 0.001) in B. forsythus proportions was also detected between supragingival (0.9%) and subgingival (15.3%) samples from adult periodontitis patients. In a separate study, patients previously treated for moderate to severe adult periodontitis were monitored over a 12-month period for evidence of disease recurrence. A significant increase in the proportions of B. forsythus was found at sites with breakdown as compared to stable sites. Breakdown was defined as loss of attachment of 2 mm or more from base line, as measured from a reference stent, or a probing depth increase of 3 mm or more. These results support the assertion that B. forsythus is associated with advanced periodontitis as well as recurrent periodontitis. Monitoring the subgingival proportions of B. forsythus may be of diagnostic value in patients on maintenance therapy. Whether B. forsythus causes periodontal disease or is a secondary colonizer of periodontal lesions remains to be determined.
TL;DR: Gingival thickness is mainly associated with tooth-related variables, and Bleeding tendency is higher if gingiva is thin.
Abstract: Objectives: Distinct periodontal phenotypes have been identified by cluster analysis, which is an explorative method with very low external validity. The aim of the present study was to investigate variance components of facial gingival thickness in young adults with mild gingivitis.
Material and methods: Thirty-three non-smoking females, 18–23 years of age, with mild or moderate plaque-induced gingivitis participated. Gingival thickness was measured at every tooth present by use of ultrasound technology to the next 0.1 mm with a lowest measurement of 0.5 mm. Periodontal probing depth and clinical attachment level were measured with a pressure-controlled probe. Gingival bleeding index was assessed after probing on a 0–2 scale, where 1 was slight, and 2 was profuse bleeding on probing. The Silness-Loe plaque index was recorded. Multilevel variance components and random intercept models were built.
Results: A 2-level (subject, tooth) variance component model of gingival thickness without any explanatory variable revealed an intercept (mean) of 0.93 ± 0.02 mm. Subject variation of gingival thickness amounted to 4.2% of the total variance. Addition of tooth- and subject-related covariates to the model revealed, after adjusting for tooth type, an association with periodontal probing depth (estimated coefficient 0.067 ± 0.025), and considerable association with average bleeding index (−0.395 ± 0.149) and plaque index (0.125 ± 0.048). Variation at the tooth level was drastically reduced; subject variation amounted to 5.2%.
Conclusion: Gingival thickness is mainly associated with tooth-related variables. Bleeding tendency is higher if gingiva is thin. Subject variability related to periodontal phenotype may add to the total variance, however, to a very low extent.
TL;DR: Examining the change of related subgingival periodontopathogens among different stage of gingivitis in adolescent may be of some value for monitoring of periodontal disease development.
Abstract: Objective
The study aims to evaluate the change of related subgingival periodontopathogens among different stage of gingivitis in adolescent and assess the relationship between periodontopathogens and the progression of periodontal inflammation.
Methods
A total of 77 subgingival plaque samples from 35 adolescent individuals were divided into three groups including gingivitis group (mild, 15 samples; moderate, 16 samples; severe, 15 samples), chronic periodontitis group (15 samples) and healthy group (15 samples). Real-time PCR was used to quantitate Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythensis, and Fusobacterium nucleatum in subgingival plaque samples.
Results
All species, except for F. nucleatum, were detected in samples from gingivitis and periodontitis groups in significantly greater number than in those from healthy group (P < 0.05). In gingivitis groups, the number of P. gingivalis, T. forsythensis, and F. nucleatum in moderate and severe gingivitis groups was significantly higher than in mild gingivitis group (P < 0.05). After merging moderate gingivitis and severe gingivitis groups into moderate-to-severe gingivitis group, the four periodontopathogens were detected in samples from periodontitis group in significantly greater number than in those from moderate-to-severe gingivitis group (P < 0.05).
Conclusion
The number of P. gingivalis, P. intermedia, T. forsythensis, and F. nucleatum in subgingival plaque increases with progression of periodontal inflammation in adolescents. Examination of periodontopathogens number in adolescents may be of some value for monitoring of periodontal disease development.
TL;DR: Prevention of periodontitis is important in diabetic children; they should receive oral hygiene instruction and visit a dentist at least twice a year.
Abstract: Children with insulin-dependent diabetes mellitus have a lower salivary flow rate, pH and buffer capacity, but a higher glucose content and peroxidase, IgA, magnesium and calcium concentration, in comparison with healthy children. Nevertheless the incidence of caries is lower than normal in diabetic children with good metabolic control. Periodontal disease usually starts at puberty as mild gingivitis with bleeding and gingival recession, and it may develop into severe periodontitis, especially in children with poor control of diabetes. Microangiopathy, impaired immune response, different bacterial microflora and collagen metabolism are involved in the pathogenesis of diabetic periodontal disease. The gingival flora is mostly composed of Gram-negative, anaerobic bacteria, while collagen has a lower solubility and is atrophic and inadequate to support the occlusion forces. For these reasons, prevention of periodontitis is important in diabetic children; they should receive oral hygiene instruction and visit a dentist at least twice a year.