The role of the microbiota in periodontal disease

The last decade has witnessed unparalleled advances in our understanding of the complexity of the oral microbiome and the compositional changes that occur in subgingival biofilms in the transition from health to gingivitis and to destructive periodontal disease. The traditional view, which has held sway for the last 2 decades, that disease is characterized by the outgrowth of a consortium, or consortia, of a limited number of potentially pathogenic organisms, has given way to an alternative paradigm. In this new view, the microbiological changes associated with disease represent whole-scale alterations to the overall microbial population structure and to the functional properties of the entire community. Thus, and in common with other microbially mediated diseases of the gastrointestinal tract, the normally balanced, symbiotic, and generally benign commensal microbiome of the tooth-associated biofilm undergoes dysbiosis to a potentially deleterious microbiota. Coincident with progress in defining the microbiology of these diseases, there have been equally important advances in our understanding of the inflammatory systems of the periodontal tissues, their control, and how inflammation may contribute both to the development of dysbiosis and, in a deregulated state, the destructive disease process. One can therefore speculate that the inflammatory response and the periodontal microbiome are in a bidirectional balance in oral health and a bidirectional imbalance in periodontitis. However, despite these clear insights into both sides of the host/microbe balance in periodontal disease, there remain several unresolved issues concerning the role of the microbiota in disease. These include, but are not limited to, the factors which determine progression from gingivitis to periodontitis in a proportion of the population, whether dysbiosis causes disease or results from disease, and the molecular details of the microbial stimulus responsible for driving the destructive inflammatory response. Further progress in resolving these issues may provide significant benefit to diagnosis, treatment, and prevention.     

High numbers of T cells in gingiva from patients with human immunodeficiency virus (HIV) infection

A quantitative, immunohistologic evaluation of CD3⁺, CD4⁺and CD8⁺ cells was carried out on gingival biopsies from 25 HIV-infected persons with gingivitis or periodontitis and 13 HIV-seronegative persons with periodontitis. CD3⁺ T cells were found in all biopsies. CD8⁺ cells were significantly more numerous and the CD4⁺/CD8⁺ ratio was significantly decreased in the gingival connective tissue of the HIV⁺ patients (P < 0.05). The number of CD4⁺ lymphocytes subjacent to the pocket epithelium was moderately lower in the HIVH patients as compared to the HIV⁺ patients (P < 0.05). HIV⁺ patients with a history of necrotizing periodontal disease had fewer CD4⁺ cells subjacent to the oral gingival epithelium than patients without such disease (P < 0.05). The general HIV-related changes in T lymphocyte numbers were therefore reflected in inflamed gingival tissues. HIV⁺ patients had, however, significantly higher CD4⁺/CD8⁺ ratios in gingiva than in peripheral blood (P < 0.05), indicating that CD4⁺ T cells are actively recruited to gingiva, even in cases of extreme CD4⁺ T lymphocytopenia.     

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目的探讨自制复方中药制剂——牙周抑菌剂局部用药治疗急性牙龈炎、牙周炎的临床疗效。方法将2006年10月至2008年4月在北京市海淀区中医医院口腔内科门诊就诊的急性牙龈炎、牙周炎患者24例(170颗患牙)随机将患者左右两侧患牙分为试验组(牙周抑菌剂组,85颗牙齿)和对照组(碘甘油组,85颗牙齿),分别局部给牙周抑菌剂或碘甘油进行治疗。治疗前后对患牙牙周相关指标[牙周探诊深度(PD)、牙龈指数(GI)、龈沟出血指数(SBI)、菌斑指数(PLI)]进行测量,并对两组治疗前后、两组治疗后的牙周相关指标及有效率情况进行比较。结果用药前后试验组、对照组各项指标自身比较,差异均具有统计学意义(均P<0.01)。用药后两组PD(t=3.257,P<0.05)、G(Iχ2=7.673,P<0.05)、SB(Iχ2=9.899,P<0.05)差异均具有统计学意义,牙周抑菌剂较碘甘油对牙周急性炎症者的PD、GI、SBI改善更明显;用药后试验组和对照组PLI差异无统计学意义(χ2=3.026,P>0.05)。试验组总有效率达75.30%,对照组总有效率为52.94%,两组差异有统计学意义(χ2=12.528,P<0.01)。结论牙周抑菌剂较碘甘油对牙周急性炎症的消炎抑菌作用更优。     

不同程度炎症的人牙龈树突状细胞的数量研究

目的：比较不同程度炎症的人牙龈树突状细胞的数量。方法：使用CD1a单克隆抗体和DC-SIGN单克隆抗体，分别对人牙龈郎格罕细胞（Langerhans cells，LCs）和真皮树突细胞（dermal dendritic cells，DDCs）作免疫组织化学染色，对正常（11例）、牙龈炎（14例）、牙周炎（15例）三组样本的两种细胞进行计数并比较。结果：LCs主要分布在牙龈上皮的基底层及棘层，高倍视野下三组样本的细胞数量分别是13±3.3、21±5.1、42±4.8（P〈0.01）；DDCs主要分布在牙龈上皮的基底膜以下，高倍视野下三组样本的细胞数量分别是27±6.3、33±5.1、76±4.8（P〈0.01）。结论：牙龈的LCs和DDCs的数量与牙周炎症发展过程有关。     

Subgingival bacterial clusters and serum antibody response as markers of extent and severity of periodontitis in adult Chinese

This study evaluated the associations between clinical, microbiological, and antibody activity manifestations of periodontitis in 123 adult rural Chinese subjects with no dental intervention. All participants were registered for full‐mouth clinical attachment level (CAL) and pocket probing depth (PD) measurements, and microbial samples were taken from four sites and analyzed for 18 different bacterial species using the ‘checkerboard’. Serum from each individual was analyzed to determine the antibody activity against the same 18 species. Exploratory factor analysis disclosed two microbial factors – Factor 1, consisting of seven species associated with periodontal health (‘early colonizers’); and Factor 2, consisting of eight species associated with periodontitis (‘putative periodontopathogens’) – which explained 87% of the variation among the microbial variables. Factor 2 was consistently associated with disease‐severity measures, whereas the ‘early colonizer’ factor was not. The antibody response showed weak or no correlations with bacterial load or with disease severity. We conclude that the bacteria investigated are resident in the subgingival plaque; that their load and proportions in the pocket may be ecologically driven; and that the antibody response is based on bacterial carrier state rather than on disease. The different antibody‐response pattern found between the individuals may suggest that each individual could be classified as a good or a weak immune responder.     

犬类动物模型在牙周病研究中的应用现状

牙周病是一种常见的感染性口腔疾病,直接危害口腔健康,是造成中国成年人失牙的最重要原因。由于牙周病临床表现复杂,为进一步探讨牙周病的发病机制、病理学特点以及治疗效果和疗效的评价,单凭临床观察是远远不够的,为此,动物模型被广泛应用。近几年来犬类动物模型广泛应用于牙周病研究,本文就犬类动物模型在牙周病研究中的应用现状进行综述。     

Gingival and periodontal ligament fibroblasts differ in their inflammatory response to viable Porphyromonas gingivalis

Scheres N, Laine ML, de Vries TJ, Everts V, van Winkelhoff AJ. Gingival and periodontal ligament fibroblasts differ in their inflammatory response to viable Porphyromonas gingivalis. J Periodont Res 2009; doi: 10.1111/j.1600‐0765.2009.01229.x © 2009 The Authors. Journal compilation © 2009 Blackwell Munksgaard Background and Objective: Porphyromonas gingivalis is an oral pathogen strongly associated with destruction of the tooth‐supporting tissues in human periodontitis. Gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDLF) are functionally different cell types in the periodontium that can participate in the host immune response in periodontitis. This study aimed to investigate the effects of viable P. gingivalis on the expression of genes associated with inflammation and bone degradation by these fibroblast subsets. Material and Methods: Primary human GF and PDLF from six healthy donors were challenged in vitro with viable P. gingivalis W83 for 6 h. Gene expression of inflammatory cytokines in GF and PDLF was analyzed using real‐time PCR, and protein expression was analyzed using ELISA. Results: Viable P. gingivalis induced a strong in vitro inflammatory response in both GF and PDLF. We found increased gene expression of interleukin (IL)‐1β, IL‐6, IL‐8, tumor necrosis factor‐α, monocyte chemotactic protein‐1 and regulated upon activation, normal T‐cell expressed and secreted (RANTES). Macrophage colony‐stimulating factor was induced and the expression of osteoprotegerin was decreased in GF, but not in PDLF. In nonchallenged cells, a higher level of expression of IL‐6 was observed in GF than in PDLF. Between individual donors there was large heterogeneity in responsiveness to P. gingivalis. Also, in each individual, either GF or PDLF was more responsive to P. gingivalis. Conclusion: Considerable heterogeneity in responsiveness to P. gingivalis exists both between GF and PDLF and between individuals, which may be crucial determinants for the susceptibility to develop periodontitis.     

Candidal infection of the gingiva in HIV-infected persons

Gingival biopsies were taken from 27 HIV (human immunodeficiency virus)-seropositive persons with gingivitis or periodontitis and 16 HIV-seronegative persons with periodontitis. Sections were stained with hematoxylin and eosin or periodic acid-Schiff. Candidal hyphae and pseudohyphae were found in the para-keratinized oral epithelium in 7 specimens from the HIV-infected patient group and in the connective tissue close to the bottom of the gingival pocket in one such specimen. No fungal invasion was found in any of the biopsies from the HIV-seronegative persons. Candidal invasion was significantly more frequent ( P <0.05) in patients with a confirmed history of necrotizing periodontal diseases (5/9) than in patients without known episodes of such diseases (3/18). The most prominent histopathologic changes observed in connection with candidal invasion comprised polymorphonuclear leucocyte infiltration of the oral gingival epithelium and numerous mitoses, some of which were located suprabasally. It is suggested that Candida albicans may contribute to the development of necrotizing periodontal diseases in HIV-infected persons.     

Modulation of clinical expression of plaque-induced gingivitis: response in aggressive periodontitis subjects

AIM: The aim of this study was to characterize the gingival inflammatory response to de novo plaque accumulation in subjects treated for aggressive periodontitis (AP). The gingival inflammatory response of the AP subjects was retrospectively compared with that of periodontally healthy individuals (PH) matched for exposure to plaque and of periodontally healthy subjects previously identified as "high responders" (HR) and "low responders" (LR). MATERIALS AND METHODS: 13 AP subjects and 26 matched PH subjects participated in a 21-day experimental gingivitis trial. Plaque index (PlI), Gingival index (GI), gingival crevicular fluid volume (GCF) and angulated bleeding score (AngBS) were recorded at days 0, 7, 14 and 21. Cumulative plaque exposure (CPE), i.e. PlI over time, was also calculated. RESULTS: GCF was significantly higher in AP compared with PH group at each observation interval (p< or =0.001). In addition, GCF was significantly higher in AP group compared with either LR or HR groups at each observation interval (p<0.001). CONCLUSIONS: These results suggest that susceptibility to gingival inflammation in response to de novo plaque accumulation may be related to susceptibility to periodontitis.     

Different treatment strategies are applied to patients with the same periodontal status in general dentistry

Objective. To analyse how general dental practitioners (GDPs) and dental hygienists judge and plan to treat patients with different periodontal conditions. Materials and methods. Seventy-seven GDPs and 50 dental hygienists in a Swedish county, Halland, participated in a questionnaire study. The response rate was 94%. The questionnaire consisted of four simulated patient cases and an attached answer sheet. The patient cases had different periodontal status, ranging from healthy to moderate bone loss with general inflammation. The clinicians judged the periodontal status as healthy or diseased. If judged as diseased the clinicians suggested a diagnosis, selected treatment options and estimated the number of treatment sessions for each patient case. The clinicians were compared to each other regarding their judgement, as healthy or diseased, diagnostics and treatment. Results. Three out of four patients were judged both as healthy and diseased by different clinicians. If judged as diseased the patients were diagnosed as having gingivitis or periodontitis. Regardless of the clinicians' former judgement and diagnostics there were no differences (p > 0.05) in the selected treatment options but there was a difference (p < 0.05) in the suggested number of treatment sessions. Conclusions. Clinicians' judgement of the same periodontal condition, as healthy or diseased, varies, which partly results in different treatment decisions considering the number of treatment sessions. The suggested number of treatment sessions varied also between clinicians even if they judged and diagnosed the condition likewise. The willingness to treat and suggested treatment options were not influenced by the variation in judgement and diagnostics.