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Journal of Clinical Periodontology Nov 2013The aim of this randomized placebo-controlled clinical trial was to evaluate the effects of Lactobacillus reuteri-containing probiotic lozenges as an adjunct to scaling... (Comparative Study)
Comparative Study Randomized Controlled Trial
AIM
The aim of this randomized placebo-controlled clinical trial was to evaluate the effects of Lactobacillus reuteri-containing probiotic lozenges as an adjunct to scaling and root planing (SRP).
MATERIAL AND METHODS
Thirty chronic periodontitis patients were recruited and monitored clinically and microbiologically at baseline, 3, 6, 9 and 12 weeks after therapy. All patients received one-stage full-mouth disinfection and randomly assigned over a test (SRP + probiotic, n = 15) or control (SRP + placebo, n = 15) group. The lozenges were used two times a day for 12 weeks.
RESULTS
At week 12, all clinical parameters were significantly reduced in both groups, while there was significantly more pocket depth reduction (p < 0.05) and attachment gain (p < 0.05) in moderate and deep pockets; more Porphyromonas gingivalis reduction was observed in the SRP + probiotic group.
CONCLUSIONS
The results indicate that oral administration of L. reuteri lozenges could be a useful adjunct to SRP in chronic periodontitis.
Topics: Adult; Aggregatibacter actinomycetemcomitans; Bacterial Load; Bacteroides; Chronic Periodontitis; Combined Modality Therapy; Dental Plaque; Dental Scaling; Disinfection; Double-Blind Method; Female; Follow-Up Studies; Fusobacterium nucleatum; Gingival Hemorrhage; Gingival Recession; Humans; Limosilactobacillus reuteri; Male; Middle Aged; Periodontal Attachment Loss; Periodontal Pocket; Placebos; Porphyromonas gingivalis; Prevotella intermedia; Probiotics; Root Planing; Tablets
PubMed: 24164569
DOI: 10.1111/jcpe.12155 -
Journal of Clinical Periodontology Aug 2008Currently, a large variety of classifications is used for periodontitis as a risk factor for other diseases. None of these classifications quantifies the amount of...
BACKGROUND
Currently, a large variety of classifications is used for periodontitis as a risk factor for other diseases. None of these classifications quantifies the amount of inflamed periodontal tissue, while this information is needed to assess the inflammatory burden posed by periodontitis.
AIM
To develop a classification of periodontitis that quantifies the amount of inflamed periodontal tissue, which can be easily and broadly applied.
MATERIAL AND METHODS
A literature search was conducted to look for a classification of periodontitis that quantified the amount of inflamed periodontal tissue. A classification that quantified the root surface area affected by attachment loss was found. This classification did not quantify the surface area of inflamed periodontal tissue, however. Therefore, an Excel spreadsheet was developed in which the periodontal inflamed surface area (PISA) is calculated using clinical Attachment Level (CAL), recessions and bleeding on probing (BOP).
RESULTS
The PISA reflects the surface area of bleeding pocket epithelium in square millimetres. The surface area of bleeding pocket epithelium quantifies the amount of inflamed periodontal tissue. A freely downloadable spreadsheet is available to calculate the PISA.
CONCLUSION
PISA quantifies the inflammatory burden posed by periodontitis and can be easily and broadly applied.
Topics: Epithelial Attachment; Gingival Hemorrhage; Gingival Recession; Humans; Inflammation; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Periodontitis; Periodontium; Tooth Root
PubMed: 18564145
DOI: 10.1111/j.1600-051X.2008.01249.x -
Proteomics. Clinical Applications Oct 2014Periodontitis is a complex immune-inflammatory disease that results from a preestablished infection in gingiva, mainly due to Gram-negative bacteria that colonize deeper... (Review)
Review
Periodontitis is a complex immune-inflammatory disease that results from a preestablished infection in gingiva, mainly due to Gram-negative bacteria that colonize deeper in gingival sulcus and latter periodontal pocket. Host inflammatory and immune responses have both protective and destructive roles. Although cytokines, prostaglandins, and proteases struggle against microbial burden, these molecules promote connective tissue loss and alveolar bone resorption, leading to several histopathological changes, namely destruction of periodontal ligament, deepening of periodontal pocket, and bone loss, which can converge to attain tooth loss. Despite the efforts of genomics, transcriptomics, proteomics/peptidomics, and metabolomics, there is no available biomarker for periodontitis diagnosis, prognosis, and treatment evaluation, which could assist on the established clinical evaluation. Nevertheless, some genes, transcripts, proteins and metabolites have already shown a different expression in healthy subjects and in patients. Though, so far, 'omics approaches only disclosed the host inflammatory response as a consequence of microbial invasion in periodontitis and the diagnosis in periodontitis still relies on clinical parameters, thus a molecular tool for assessing periodontitis lacks in current dental medicine paradigm. Saliva and gingival crevicular fluid have been attracting researchers due to their diagnostic potential, ease, and noninvasive nature of collection. Each one of these fluids has some advantages and disadvantages that are discussed in this review.
Topics: Humans; Periodontitis
PubMed: 24828325
DOI: 10.1002/prca.201400028 -
International Journal of Molecular... Aug 2022(), one of the 'red‑complex' perio‑pathogens known to play a critical role in the development of periodontitis, has been used in various animal models to mimic...
(), one of the 'red‑complex' perio‑pathogens known to play a critical role in the development of periodontitis, has been used in various animal models to mimic human bacteria‑induced periodontitis. In order to achieve a more realistic animal model of human infection, the present study investigated whether repeated small‑volume topical applications of directly into the gingival pocket can induce local infection, including periodontitis and systemic vascular inflammation in wild‑type mice. Freshly cultured was topically applied directly into the gingival pocket of the second molars for 5 weeks (3 times/week). After the final application, the mice were left in cages for 4 or 8 weeks and sacrificed. The status of colony formation in the pocket, gingival inflammation, alveolar bone loss, the expression levels of pro‑inflammatory cytokines in the serum and aorta, the presence of anti‑ lipopolysaccharide (LPS) and gingipain (Kpg and RgpB) antibodies in the serum, as well as the accumulation of LPS and gingipain aggregates in the gingiva and arterial wall were evaluated. The topical application of into the gingival pocket induced the following local and systemic pathohistological changes in mice when examined at 4 or 8 weeks after the final topical application: colonization in the majority of gingival pockets; increased gingival pocket depths; gingival inflammation indicated by the increased expression of TNF‑α, IL‑6 and IL‑1β; significant loss of alveolar bone at the sites of topical application; and increased levels of pro‑inflammatory cytokines, such as TNF‑α, IL‑1β, IL‑17, IL‑13, KC and IFN‑γ in the serum in comparison to those from mice receiving PBS. In addition, the application/colonization model induced anti‑ LPS and gingipain antibodies in serum, as well as the accumulation of LPS and gingipain aggregates in the gingivae and arterial walls. To the best of our knowledge, this mouse model represents the first example of creating a more sustained local infection in the gingival tissues of wild‑type mice and may prove to be useful for the investigation of the more natural and complete pathogenesis of the bacteria in the development of local oral and systemic diseases, such as atherosclerosis. It may also be useful for the determination of a treatment/prevention/efficacy model associated with ‑induced colonization periodontitis in mice.
Topics: Animals; Cytokines; Disease Models, Animal; Gingipain Cysteine Endopeptidases; Gingival Pocket; Inflammation; Lipopolysaccharides; Mice; Periodontitis; Porphyromonas gingivalis; Tumor Necrosis Factor-alpha
PubMed: 35703359
DOI: 10.3892/ijmm.2022.5159 -
Neurosurgical Review Apr 2020Oral bacteria DNA has been found in intracranial aneurysms (IA) and a high prevalence of periodontitis was reported in IA patients. We investigated whether periodontitis...
Oral bacteria DNA has been found in intracranial aneurysms (IA) and a high prevalence of periodontitis was reported in IA patients. We investigated whether periodontitis associates with IA formation and aneurysmal subarachnoid hemorrhage (aSAH). First, we compared in a case-control setting the prevalence of periodontal disease in IA patients (42 unruptured IA, 34 ruptured IA) and in age- and gender-matched controls (n = 70) from the same geographical area (Health 2000 Survey, BRIF8901). Next, we investigated whether periodontitis at baseline associated with aSAH in a 13-year follow-up study of 5170 Health 2000 Survey participants. Follow-up data was obtained from national hospital discharge and cause of death registries. Univariate analysis, logistic regression, and Cox-regression were used. Periodontitis (≥ 4mm gingival pocket) and severe periodontitis (≥ 6mm gingival pocket) were found in 92% and 49% of IA patients respectively and associated with IAs (OR 5.3, 95%CI 1.1-25.9, p < 0.000 and OR 6.3, 95%CI 1.3-31.4, p < 0.001, respectively). Gingival bleeding had an even stronger association, especially if detected in 4-6 teeth sextants (OR 34.4, 95%CI 4.2-281.3). Severe periodontitis in ≥ 3 teeth or gingival bleeding in 4-6 teeth sextants at baseline increased the risk of aSAH during follow-up (HR 22.5, 95%CI 3.6-139.5, p = 0.001 and HR 8.3, 95%CI 1.5-46.1, p = 0.015, respectively). Association of periodontitis and gingival bleeding with risk of IA development and aSAH was independent of gender, smoking status, hypertension, or alcohol abuse. Periodontitis and gingival bleeding associate with increased risk for IA formation and eventual aSAH. Further epidemiological and mechanistic studies are indicated.
Topics: Adult; Aged; Aneurysm, Ruptured; Case-Control Studies; Female; Follow-Up Studies; Gingival Hemorrhage; Humans; Intracranial Aneurysm; Logistic Models; Male; Middle Aged; Periodontitis; Prevalence; Registries; Risk Factors; Smoking; Subarachnoid Hemorrhage; Young Adult
PubMed: 30972514
DOI: 10.1007/s10143-019-01097-1 -
Cureus Mar 2022This case report describes Clark's technique of vestibuloplasty to treat shallow vestibule and, in addition, the use of free gingival autograft to augment attached...
This case report describes Clark's technique of vestibuloplasty to treat shallow vestibule and, in addition, the use of free gingival autograft to augment attached gingiva to treat Miller's recession. Vestibuloplasty is performed to deepen a shallow vestibule. Different vestibuloplasty techniques are used to deepen the shallow vestibule by modifying the soft tissue attachment. A 29-year-old male presented to the Department of Periodontics and Oral Implantology, Regional Dental College, Guwahati, India with the chief complaint of bleeding from the lower anterior along with the gingival recession. Maintenance of regular oral hygiene was an added hindrance. The combined technique of vestibuloplasty and use of free gingival graft was performed to achieve dual benefits of increasing the vestibular depth and attainment of a thick gingival phenotype.
PubMed: 35510014
DOI: 10.7759/cureus.23642 -
Frontiers in Oral Health 2023The purpose of this narrative review is to highlight the importance of microbial metabolites in the pathogenesis of periodontal diseases. These diseases, involving... (Review)
Review
The purpose of this narrative review is to highlight the importance of microbial metabolites in the pathogenesis of periodontal diseases. These diseases, involving gingivitis and periodontitis are inflammatory conditions initiated and maintained by the polymicrobial dental plaque/biofilm. Gingivitis is a reversible inflammatory condition while periodontitis involves also irreversible destruction of the periodontal tissues including the alveolar bone. The inflammatory response of the host is a natural reaction to the formation of plaque and the continuous release of metabolic waste products. The microorganisms grow in a nutritious and shielded niche in the periodontal pocket, protected from natural cleaning forces such as saliva. It is a paradox that the consequences of the enhanced inflammatory reaction also enable more slow-growing, fastidious, anaerobic bacteria, with often complex metabolic pathways, to colonize and thrive. Based on complex food chains, nutrient networks and bacterial interactions, a diverse microbial community is formed and established in the gingival pocket. This microbiota is dominated by anaerobic, often motile, Gram-negatives with proteolytic metabolism. Although this alternation in bacterial composition often is considered pathologic, it is a natural development that is promoted by ecological factors and not necessarily a true "dysbiosis". Normal commensals are adapting to the gingival crevice when tooth cleaning procedures are absent. The proteolytic metabolism is highly complex and involves a number of metabolic pathways with production of a cascade of metabolites in an unspecific manner. The metabolites involve short chain fatty acids (SCFAs; formic, acetic, propionic, butyric, and valeric acid), amines (indole, scatole, cadaverine, putrescine, spermine, spermidine) and gases (NH, CO, NO, HS, H). A homeostatic condition is often present between the colonizers and the host response, where continuous metabolic fluctuations are balanced by the inflammatory response. While it is well established that the effect of the dental biofilm on the host response and tissue repair is mediated by microbial metabolites, the mechanisms behind the tissue destruction (loss of clinical attachment and bone) are still poorly understood. Studies addressing the functions of the microbiota, the metabolites, and how they interplay with host tissues and cells, are therefore warranted.
PubMed: 37388417
DOI: 10.3389/froh.2023.1210200 -
The Japanese Dental Science Review Nov 2020The aim was to determine whether there is a difference in the periodontal aspect (gingival recession, probing pocket depth) of the palatally displaced canine (PDC)... (Review)
Review
The aim was to determine whether there is a difference in the periodontal aspect (gingival recession, probing pocket depth) of the palatally displaced canine (PDC) compared to the contralateral canine. Also, from a surgical perspective, sought to determine whether there is a difference (surgical duration, postoperative pain) between the surgical techniques. The word combinations were adapted for each electronic database: PubMed, LILACS, Scopus, Web of Science, Cochrane Library and gray literature. Studies that met the following criteria were considered eligible: (P) Patients who received orthodontic-surgical treatment for correction of PDC; (I) Performing orthodontic-surgical treatment for traction of the PDC; (C) Comparison of the tractioned canine with its contralateral or between the two techniques; (O) Gingival recession, probing pocket depth, postoperative complications and surgical duration; (S) Randomized and nonrandomized clinical studies or observational studies. The overall prevalence of gingival recession was estimated to be 10.53% [95% CI, 3.87% - 25.59%; I = 88%]. No statistically significant difference (p > 0.05) was found between the means of the variables gingival recession, probing pocket depth and surgical duration. The evidence suggests that traction of palatally displaced canines can be considered a reliable and acceptable procedure.
PubMed: 33294059
DOI: 10.1016/j.jdsr.2020.10.001 -
International Journal of Dental Hygiene Nov 2014To assess gingival recession (GR) in manual and power toothbrush users and evaluate the relationship between GR and gingival abrasion scores (GA). (Comparative Study)
Comparative Study Observational Study
OBJECTIVE
To assess gingival recession (GR) in manual and power toothbrush users and evaluate the relationship between GR and gingival abrasion scores (GA).
METHODS
This was an observational (cross-sectional), single-centre, examiner-blind study involving a single-brushing exercise, with 181 young adult participants: 90 manual brush users and 91 oscillating-rotating power brush users. Participants were assessed for GR and GA as primary response variables. Secondary response variables were the level of gingival inflammation, plaque score reduction and brushing duration. Pearson correlation was used to describe the relationship between number of recession sites and number of abrasions. Prebrushing (baseline) and post-brushing GA and plaque scores were assessed and differences analysed using paired tests. Two-sample t-test was used to analyse group differences; ancova was used for analyses of post-brushing changes with baseline as covariate.
RESULTS
Overall, 97.8% of the study population had at least one site of ≥1 mm of gingival recession. For the manual group, this percentage was 98.9%, and for the power group, this percentage was 96.7% (P = 0.621). Post-brushing, the power group showed a significantly smaller GA increase than the manual group (P = 0.004); however, there was no significant correlation between number of recession sites and number of abrasions for either group (P ≥ 0.327).
CONCLUSIONS
Little gingival recession was observed in either toothbrush user group; the observed GR levels were comparable. Lower post-brushing gingival abrasion levels were seen in the power group. There was no correlation between gingival abrasion as a result of brushing and the observed gingival recession following use of either toothbrush.
Topics: Adolescent; Adult; Coloring Agents; Cross-Sectional Studies; Dental Plaque; Dental Plaque Index; Equipment Design; Female; Gingiva; Gingival Recession; Gingivitis; Humans; Male; Periodontal Index; Periodontal Pocket; Single-Blind Method; Time Factors; Toothbrushing; Young Adult
PubMed: 24871587
DOI: 10.1111/idh.12085 -
The Open Dentistry Journal 2016Non-Inflammatory Destructive Periodontal Disease (NIDPD), is a severe destructive periodontal disease, that is characterized by the attachment loss and alveolar bone...
BACKGROUND
Non-Inflammatory Destructive Periodontal Disease (NIDPD), is a severe destructive periodontal disease, that is characterized by the attachment loss and alveolar bone loss, without signs of the gingival inflammation, and the periodontal pocket development.
OBJECTIVE
Despite the fact that various cases of NIDPD have been reported; their etiology and disease evolution is still indefinite, and therefore, are open for discussion.
METHOD
An NIDPD case was studied in order to demonstrate features of the disease, and discuss the possible etiology and treatment.
RESULTS
In this clinical case, the etiology of NIDPD seems to be an association of endogenous opportunist bacteria with anatomical aspects, occlusion pattern, emotional stress and mouth breathing condition.
CONCLUSION
In spite of all cases described in the literature are comparable and may have similar etiology as related in this clinical case, additional research is needed to identify and clarify the role of the etiologic factors which determine the disease.
PubMed: 27053968
DOI: 10.2174/1874210601610010050