A classification scheme for periodontal and peri-implant diseases and conditions is necessary for clinicians to properly diagnose and treat patients as well as for scientists to investigate etiology, pathogenesis, natural history, and treatment of the diseases and conditions. This paper summarizes the proceedings of the World Workshop on the Classification of Periodontal and Peri-implant Diseases and Conditions. The workshop was co-sponsored by the American Academy of Periodontology (AAP) and the European Federation of Periodontology (EFP) and included expert participants from all over the world. Planning for the conference, which was held in Chicago on November 9 to 11, 2017, began in early 2015. An organizing committee from the AAP and EFP commissioned 19 review papers and four consensus reports covering relevant areas in periodontology and implant dentistry. The authors were charged with updating the 1999 classification of periodontal diseases and conditions and developing a similar scheme for peri-implant diseases and conditions. Reviewers and workgroups were also asked to establish pertinent case definitions and to provide diagnostic criteria to aid clinicians in the use of the new classification. All findings and recommendations of the workshop were agreed to by consensus. This introductory paper presents an overview for the new classification of periodontal and peri-implant diseases and conditions, along with a condensed scheme for each of four workgroup sections, but readers are directed to the pertinent consensus reports and review papers for a thorough discussion of the rationale, criteria, and interpretation of the proposed classification. Changes to the 1999 classification are highlighted and discussed. Although the intent of the workshop was to base classification on the strongest available scientific evidence, lower level evidence and expert opinion were inevitably used whenever sufficient research data were unavailable. The scope of this workshop was to align and update the classification scheme to the current understanding of periodontal and peri-implant diseases and conditions. This introductory overview presents the schematic tables for the new classification of periodontal and peri-implant diseases and conditions and briefly highlights changes made to the 1999 classification. It cannot present the wealth of information included in the reviews, case definition papers, and consensus reports that has guided the development of the new classification, and reference to the consensus and case definition papers is necessary to provide a thorough understanding of its use for either case management or scientific investigation. Therefore, it is strongly recommended that the reader use this overview as an introduction to these subjects. Accessing this publication online will allow the reader to use the links in this overview and the tables to view the source papers (Table 1).

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A new classification scheme for periodontal and peri-implant diseases and conditions - Introduction and key changes from the 1999 classification.

Periodontal diseases (PD) are chronic infectious inflammatory diseases characterized by the destruction of tooth-supporting structures, being the presence of periodontopathogens required, but not sufficient, for disease development. As a general rule, host inflammatory mediators have been associated with tissue destruction, while anti-inflammatory mediators counteract and attenuate disease progression. With the discovery of several T-cell subsets bearing distinct immunoregulatory properties, this pro- vs. anti-inflammatory scenario became more complex, and a series of studies has hypothesized protective or destructive roles for Th1, Th2, Th17, and Treg subpopulations of polarized lymphocytes. Interestingly, the “protective vs. destructive” archetype is usually considered in a framework related to tissue destruction and disease progression. However, it is important to remember that periodontal diseases are infectious inflammatory conditions, and recent studies have demonstrated that cytokines (TNF-α and IF...

Destructive and Protective Roles of Cytokines in Periodontitis: A Re-appraisal from Host Defense and Tissue Destruction Viewpoints

Periodontal diseases are initiated by bacterial species living in polymicrobial biofilms at or below the gingival margin and progress largely as a result of the inflammation elicited by specific subgingival species. In the past few decades, efforts to understand the periodontal microbiota have led to an exponential increase in information about biofilms associated with periodontal health and disease. In fact, the oral microbiota is one of the best-characterized microbiomes that colonize the human body. Despite this increased knowledge, one has to ask if our fundamental concepts of the etiology and pathogenesis of periodontal diseases have really changed. In this article we will review how our comprehension of the structure and function of the subgingival microbiota has evolved over the years in search of lessons learned and unlearned in periodontal microbiology. More specifically, this review focuses on: (i) how the data obtained through molecular techniques have impacted our knowledge of the etiology of periodontal infections; (ii) the potential role of viruses in the etiopathogenesis of periodontal diseases; (iii) how concepts of microbial ecology have expanded our understanding of host-microbe interactions that might lead to periodontal diseases; (iv) the role of inflammation in the pathogenesis of periodontal diseases; and (v) the impact of these evolving concepts on therapeutic and preventive strategies to periodontal infections. We will conclude by reviewing how novel systems-biology approaches promise to unravel new details of the pathogenesis of periodontal diseases and hopefully lead to a better understanding of their mechanisms.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/prd.12010

Lessons learned and unlearned in periodontal microbiology.

Periodontitis is an inflammatory disease involving the destruction of both soft and hard tissue in the periodontal region. Although dysbiosis of the local microbial community initiates local inflammation, over-activation of the host immune response directly activates osteoclastic activity and alveolar bone loss. Many studies have reported on the cytokine network involved in periodontitis and its crucial and pleiotropic effect on the recruitment of specific immunocytes, control of pathobionts and induction or suppression of osteoclastic activity. Nonetheless, particularities in the stimulation of pathogens in the oral cavity that lead to the specific and complex periodontal cytokine network are far from clarified. Thus, in this review, we begin with an up-to-date aetiological hypothesis of periodontal disease and summarize the roles of cytokines in the host immune response. In addition, we also summarize the latest cytokine-related therapeutic measures for periodontal disease.

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The cytokine network involved in the host immune response to periodontitis

The periodontal diseases range from the relatively benign form of periodontal disease known as gingivitis, to chronic and aggressive forms of periodontal disease, all of which not only threaten the dentition but may also be a threat to general health (72). All forms of inflammatory periodontal disease are associated with chronic inflammation, resulting in destruction of the periodontal ligament and bone. If left untreated, significant tissue damage occurs; the affected teeth can become loose and may be lost if the disease continues to be active. The periodontal diseases are very prevalent, with up to 90% of the adult population suffering from gingivitis, 60% having chronic periodontitis and 5–15% having aggressive periodontitis (72). Histologically and biochemically the periodontal lesions of patients with chronic and aggressive periodontitis appear to be similar. While there may be some differences in the cellular infiltrate between these two diseases (discussed elsewhere in this edition of Periodontology 2000), the molecular mediators and pathologic processes are generally the same. The only differences between chronic periodontitis and aggressive periodontitis with regard to tissue destruction appear to be perhaps the magnitude, sequelae and control of the response. Otherwise the mechanisms are remarkably similar. While a great deal of focus has been on managing the inflammation in the gingival tissues, advances in our understanding of bone metabolism are opening up new avenues of understanding regarding the pathologic bone loss in periodontitis. This knowledge, together with the development of novel drugs that can inhibit bone loss ⁄ destruction, provides us with opportunities to target not only soft tissue inflammation but also the destructive bone loss seen in periodontitis. This review aims to demonstrate that, in the future, periodontal treatments will not only target the inflammatory response but will also utilize adjunct agents to prevent alveolar bone loss associated with progressing periodontitis.

Mechanisms and control of pathologic bone loss in periodontitis

Background: The aim of this study was to evaluate the influence of anti-tumor necrosis factor-alpha (TNF-a) therapy on the clinical and immunologic parameters of the periodontium. Methods: Ten patients with rheumatoid arthritis (RA) who routinely received infusions of infliximab, 200 mg (RA+), 10 patients with RA without anti-TNF-a therapy (RA-), and 10 healthy controls (C) were included. Clinical parameters, including the plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment loss (AL), and bleeding on probing (BOP), were assessed, and total gingival crevicular fluid (GCF) TNF-a level was determined using enzyme-linked immunosorbent assay. Analysis of variance with Scheffe modification and the Pearson correlation test were used for statistical analysis. Results: The ages of the patients ranged from 22 to 76 years (mean, 50.73 – 9.1 years). The mean PI was similar among the groups. However, mean inflammatory parameters in the three groups varied significantly; GI was greater in the RA- group compared to RA+ and C groups (P = 0.0042). The RA+ group exhibited less BOP than RA- and C groups (21.1% – 3.0%, 45.9% – 6.2%, and 39.1% – 7.2%, respectively; P = 0.0146). The mean PD in the RA+ group was shallower than in RA- and C groups (3.22 – 0.13 mm, 3.85 – 0.22 mm, and 3.77 – 0.20 mm, respectively; P = 0.055). Clinical AL in the RA+ group was lower than in RA- and C groups (3.68 – 0.11 mm, 4.52 – 0.26 mm, and 4.35 – 0.24 mm, respectively; P = 0.0273). TNF-a levels in the GCF of the RA+ group were the lowest compared to RA- and C groups (0.663, 1.23, and 0.949 ng/site, respectively; P = 0.0401). A significant positive correlation was found between TNF-a levels in the GCF and clinical AL (r = 0.448; P = 0.0283). Conclusions: Patients with RA receiving anti-TNF-a medication had lower periodontal indices and GCF TNF-a levels. Thus, suppression of proinflammatory cytokines might prove beneficial in suppressing periodontal diseases. J Periodontol 2009;80:1414-1420.

Anti-Tumor Necrosis Factor-Alpha Therapy and Periodontal Parameters in Patients With Rheumatoid Arthritis

Background: The aim of this study is to evaluate the effect of autoimmune diseases (AIs), as well as anti-tumor necrosis factor-α (TNF-α) therapy on the clinical and immunologic parameters of the periodontium.Methods: Thirty-six AI patients (12 rheumatoid arthritis [RA], 12 psoriatic arthritis, and 12 systemic sclerosis) were recruited together with 12 healthy (H) and 10 RA patients receiving anti-TNF-α therapy (RA+). Periodontal indices including plaque index, gingival index (GI), probing depth (PD), and bleeding on probing (BOP) were measured, and gingival crevicular fluid (GCF) was collected from five deepest pockets using papers strips. The TNF-α level was analyzed using enzyme-linked immunosorbent assay. Analysis of variance test was used for statistical comparison between groups, whereas Pearson linear correlation coefficient test was used to examine the association between TNF-α and periodontal status indices.Results: The three AI subgroups were very similar in clinical and immunologic parameters. ...

Periodontal condition of patients with autoimmune diseases and the effect of anti-tumor necrosis factor-α therapy

Aim

To evaluate (clinically, histologically, and histo-morphometrically) the use of composite materials (Biphasic calcium sulphate [BCS] with β Tri-Calcium Phosphate (β-TCP) and Hydroxyapatite [HA]) in extraction socket sites and compare it to un-disturbed natural healing.



Material and Methods

Prospective clinical trial of 36 patients (40 extraction sockets) were randomly assigned to either test or control group. Alveolar ridge horizontal dimension was measured in the middle of the socket at crest and 3 and 6 mm subcrestally. Crestal vertical height was measured at baseline surgery and at 4 month re-entry, at which time bone core biopsies were harvested from the center of the edentulous ridge. Histo-morphometric evaluation of the samples was performed using hematoxylin & eosin stains and morphometric software.



Results

The change in horizontal ridge width was higher in the control compared to the experimental group: 2.28 ± 2.36 mm versus 0.03 ± 2.32 mm (p = .007) at −3 mm and 2.28 ± 2.43 versus 0.035 ± 3.05 (p = .02) at −6 mm, for the experimental and control sites, respectively. The vertical distance form bone crest to neighboring horizontal line interconnecting the neighboring teeth was minimal in both groups (0.307 ± 2.01 mm versus 0.14 ± 2.03 mm [p = 0.41]). Residual scaffolds occupied 15.99 ± 11.4% of the volume in the grafted (test) sites while bone area fraction was not statistically different among the groups (47.7 ± 10.6% versus 52.6 ± 11.6%, test versus control, respectively p = .39). The percentage of connective tissue in the control group was significantly higher that test group (36.3 ± 19.4% versus 46.7 ± 10.6% test versus control, respectively, p = .013).



Conclusion

Ridge preservation technique using a combination of two synthetic bone grafts β-TCP and HA with BCS resulted in greater stability in the horizontal dimension after 4 months.

Ridge Preservation Using Composite Alloplastic Materials: A Randomized Control Clinical and Histological Study in Humans

Purpose To compare dimensional changes and bone quality of two different grafting materials used for socket preservation. Materials and methods Thirty-three patients requiring extraction were recruited and randomly assigned to receive: biphasic calcium sulfate/ hydroxyapatite (BCS/HA); bovine derived xenograft (BDX) or no grafting (Control). Ridge width (at -3 and -6 mm) and vertical distance from a stent were measured at the time of extraction/grafting. Measurements were repeated at reentry and core biopsies were harvested. Results Baseline vertical distance for the BDX, C and BCS/HA groups were 7.45 ± 3.1, 7.69 ± 4.2, and 6.75 ± 3.5 mm, respectively (P = .830). Post-op, C group had greater vertical loss (1.71 ± 0.4 mm) compared to BCS/HA (0.65 ± 0.5) and BDX (0.25 ± 0.2 mm), P = .059. Mean baseline width at -3 mm was 8.69 ± 1.1 mm, 8.31 ± 1.4 mm, and 9.0 ± 1.1 mm, respectively (P = .509). Post-op, this width was reduced by 2.96 ± 0.3 mm (C), 1.56 ± 0.4 mm (BDX), and 0.5 ± 0.4 mm (BCS/HA), P = .001. Mean ridge width at -6 mm for the C (6.5 ± 1.7 mm) was significantly smaller than BCS/HA (7.95 ± 2.8 mm) and BDX (8.85 ± 1.9 mm), P = .043. Histologically, the BDX group had greater residual scaffold material and less vital bone compared to the BCS/HA group. Pain scores were relatively low for all groups. Conclusions BCS/HA may be used for socket preservation with similar or better results compared to BDX. The significance of greater residual scaffold found in the BDX group is yet to be determined.

Prospective randomized controlled clinical trial to compare hard tissue changes following socket preservation using alloplasts, xenografts vs no grafting: Clinical and histological findings

Background: A new photometric method is introduced for assessment of gingival condition and changes after periodontal therapyMethods: Clinical data (probing depth [PD], plaque index [PI], gingival index [GI], bleeding on probing [BOP], and clinical attachment level) and photographs from 53 participants (26 males and 27 females) undergoing initial periodontal treatment were used for this analysis Each maxillary anterior area was photographed before and 3 months after treatment Digital image analysis was performed around one incisional tooth, and color data were expressed in terms of L*, a*, and b* values in accordance with the CIELAB color space Non-parametric Mann–Whitney U test was used for within-group comparisons of disease resolution, as well as means and standard deviations of clinical parameters and ΔL, Δa, and Δb values from baseline to re-evaluationResults: Significant reduction in mean PI, GI, PD, and BOP were found after treatment in all groups (P <0001) Significant differences (P <005) 

Yaniv Mayer

Papers

Anti-Tumor Necrosis Factor-Alpha Therapy and Periodontal Parameters in Patients With Rheumatoid Arthritis

Periodontal condition of patients with autoimmune diseases and the effect of anti-tumor necrosis factor-α therapy

Ridge Preservation Using Composite Alloplastic Materials: A Randomized Control Clinical and Histological Study in Humans

Prospective randomized controlled clinical trial to compare hard tissue changes following socket preservation using alloplasts, xenografts vs no grafting: Clinical and histological findings

Photometric CIELAB Analysis of the Gingiva: A Novel Approach to Assess Response to Periodontal Therapy.