Journal of Clinical Periodontology 

About: Journal of Clinical Periodontology is an academic journal published by Wiley-Blackwell. The journal publishes majorly in the area(s): Periodontitis & Gingivitis. It has an ISSN identifier of 0303-6979. Over the lifetime, 6094 publications have been published receiving 392489 citations.

Microbial complexes in subgingival plaque

Abstract: It has been recognized for some time that bacterial species exist in complexes in subgingival plaque. The purpose of the present investigation was to attempt to define such communities using data from large numbers of plaque samples and different clustering and ordination techniques. Subgingival plaque samples were taken from the mesial aspect of each tooth in 185 subjects (mean age 51 +/- 16 years) with (n = 160) or without (n = 25) periodontitis. The presence and levels of 40 subgingival taxa were determined in 13,261 plaque samples using whole genomic DNA probes and checkerboard DNA-DNA hybridization. Clinical assessments were made at 6 sites per tooth at each visit. Similarities between pairs of species were computed using phi coefficients and species clustered using an averaged unweighted linkage sort. Community ordination was performed using principal components analysis and correspondence analysis. 5 major complexes were consistently observed using any of the analytical methods. One complex consisted of the tightly related group: Bacteroides forsythus, Porphyromonas gingivalis and Treponema denticola. The 2nd complex consisted of a tightly related core group including members of the Fusobacterium nucleatum/periodonticum subspecies, Prevotella intermedia, Prevotella nigrescens and Peptostreptococcus micros. Species associated with this group included: Eubacterium nodatum, Campylobacter rectus, Campylobacter showae, Streptococcus constellatus and Campylobacter gracilis. The 3rd complex consisted of Streptococcus sanguis, S. oralis, S. mitis, S. gordonii and S. intermedius. The 4th complex was comprised of 3 Capnocytophaga species, Campylobacter concisus, Eikenella corrodens and Actinobacillus actinomycetemcomitans serotype a. The 5th complex consisted of Veillonella parvula and Actinomyces odontolyticus. A. actinomycetemcomitans serotype b, Selenomonas noxia and Actinomyces naeslundii genospecies 2 (A. viscosus) were outliers with little relation to each other and the 5 major complexes. The 1st complex related strikingly to clinical measures of periodontal disease particularly pocket depth and bleeding on probing.

Dimensional ridge alterations following tooth extraction. An experimental study in the dog

Abstract: Objective: To study dimensional alterations of the alveolar ridge that occurred following tooth extraction as well as processes of bone modelling and remodelling associated with such change. Material and Methods: Twelve mongrel dogs were included in the study. In both quadrants of the mandible incisions were made in the crevice region of the 3rd and 4th premolars. Minute buccal and lingual full thickness flaps were elevated. The four premolars were hemi-sected. The distal roots were removed. The extraction sites were covered with the mobilized gingival tissue. The extractions of the roots and the sacrifice of the dogs were staggered in such a manner that all dogs contributed with sockets representing 1, 2, 4 and 8 weeks of healing. The animals were sacrificed and tissue blocks containing the extraction socket were dissected, decalcified in EDTA, embedded in paraffin and cut in the buccal–lingual plane. The sections were stained in haematoxyline–eosine and examined in the microscope. Results: It was demonstrated that marked dimensional alterations occurred during the first 8 weeks following the extraction of mandibular premolars. Thus, in this interval there was a marked osteoclastic activity resulting in resorption of the crestal region of both the buccal and the lingual bone wall. The reduction of the height of the walls was more pronounced at the buccal than at the lingual aspect of the extraction socket. The height reduction was accompanied by a “horizontal” bone loss that was caused by osteoclasts present in lacunae on the surface of both the buccal and the lingual bone wall. Conclusions: The resorption of the buccal/lingual walls of the extraction site occurred in two overlapping phases. During phase 1, the bundle bone was resorbed and replaced with woven bone. Since the crest of the buccal bone wall was comprised solely of bundle this modelling resulted in substantial vertical reduction of the buccal crest. Phase 2 included resorption that occurred from the outer surfaces of both bone walls. The reason for this additional bone loss is presently not understood.

The interleukin-1 genotype as a severity factor in adult periodontal disease

Abstract: Although specific bacteria, dental plaque, and age are associated with periodontal disease, there are currently no reliable predictors of periodontitis severity. Studies in twins have suggested a genetic contribution to the pathogenesis of periodontitis, but previous attempts to identify genetic markers have been unsuccessful. The pro-inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF alpha) are key regulators of the host responses to microbial infection. IL-1 is also a major modulator of extracellular matrix catabolism and bone resorption. We report a specific genotype of the polymorphic IL-1 gene cluster that was associated with severity of periodontitis in non-smokers, and distinguished individuals with severe periodontitis from those with mild disease (odds ratio 18.9 for ages 40-60 years). Functionally, the specific periodontitis-associated IL-1 genotype comprises a variant in the IL-1B gene that is associated with high levels of IL-1 production. In smokers severe disease was not correlated with genotype. In this study, 86.0% of the severe periodontitis patients were accounted for by either smoking or the IL-1 genotype. This study demonstrates that specific genetic markers, that have been associated with increased IL-1 production, are a strong indicator of susceptibility to severe periodontitis in adults.

Peri-implant diseases: Consensus Report of the Sixth European Workshop on Periodontology

Abstract: Issues related to peri-implant disease were discussed. It was observed that the most common lesions that occur, i.e. peri-implant mucositis and peri-implantitis are caused by bacteria. While the lesion of peri-implant mucositis resides in the soft tissues, peri-implantitis also affects the supporting bone. Peri-implant mucositis occurs in about 80% of subjects (50% of sites) restored with implants, and peri-implantitis in between 28% and 56% of subjects (12-40% of sites). A number of risk indicators were identified including (i) poor oral hygiene, (ii) a history of periodontitis, (iii) diabetes and (iv) smoking. It was concluded that the treatment of peri-implant disease must include anti-infective measures. With respect to peri-implant mucositis, it appeared that non-surgical mechanical therapy caused the reduction in inflammation (bleeding on probing) but also that the adjunctive use of antimicrobial mouthrinses had a positive effect. It was agreed that the outcome of non-surgical treatment of peri-implantitis was unpredictable. The primary objective of surgical treatment in peri-implantitis is to get access to the implant surface for debridement and decontamination in order to achieve resolution of the inflammatory lesion. There was limited evidence that such treatment with the adjunctive use of systemic antibiotics could resolve a number of peri-implantitis lesions. There was no evidence that so-called regenerative procedures had additional beneficial effects on treatment outcome.

New attachment following surgical treatment of human periodontal disease.

Abstract: The present experiment was undertaken to test the hypothesis that new connective tissue attachment may form on a previously periodontitis involved root surface provided cells originating from the periodontal ligament are enabled to repopulate the root surface during healing. A mandibular incisor with advanced periodontal disease of long standing (the distance between the cemento-enamel junction and the alveolar bone crest was 9 mm) was subjected to periodontal surgery using a technique which during healing prevented the dentogingival epithelium and the gingival connective tissue from reaching contact with the curetted root surface. Preference was hereby given to the periodontal ligament cells to repopulate the previously diseased root surface. After 3 months of healing a block biopsy containing the incisor and surrounding tissue was sampled. The histological analysis revealed that new cementum with inserting principal fibers had formed on the previously diseased root surface. This new attachment extended in coronal direction to a level 5 mm coronal to the alveolar bone crest. This finding suggests that new attachment can be achieved by cells originating from the periodontal ligament and demonstrates that the concept that the periodontitis affected root surface is a major preventive factor for new attachment is invalid.