With hybridization probes derived from the fimbrial locus of Porphyromonas gingivalis strain 381, fimA 381 ' restriction fragment length polymorphisms (RFLPs) were examined at the fimbrillin locus in 39 human and animal strains of this species. The 39 strains were subdivided into nine RFLP groups (I-IX) after genomic digests were probed with the internal coding sequence of the fimA 381 gene. Thirty-three strains showed one or more AluI fragments of moderate-to-high homology (≥77%) with the internal coding sequence of fimA 381 . These strains were distributed into the first seven RFLP groups, based solely on the size of the major hybridizing AluI fragment. Five human strains (RFLP Group VIII) had only one Alu I fragment that hybridized very poorly with this probe. One animal strain did not have homology at all (RFLP Group IX). When all AluI fragments that hybridized with fimA 381 were analyzed, RFLP groups I-VIII were further differentiated into 25 distinct RFLP patterns. Hybridizations were also performed with the internal coding sequence of fimA 381 to probe PstI genomic digests of selected strains that appeared to have lesser homology with fimA 381 . These hybridizations were performed to determine the level and location of the region of poor homology within the fimA genes of these strains. The results suggested that fimbrial coding sequences are more commonly conserved between these strains in the 5'-region of the fimA locus (≥92% sequence homology). However, the five human strains of RFLP Group VIII had only one PstI fragment that hybridized very poorly with a probe derived from fimA 381 coding sequence, and this sequence homology (only > 66%) was located in the central or 3'-end of the fimA gene. The 5'-region of the fimA allele in Group VIII strains did not have any detectable sequence homology. In contrast, the Group VIII strains were highly homologous with the sequences flanking the fimA 381 gene. This indicates that these strains do possess a fimA allele at the same chromosomal location as fimA 381 .
While the evidence shows that periodontitis and atherosclerotic cardiovascular diseases are linked, the reasons behind this association are still being investigated.
Abstract Objective To assess in a population deprived from regular dental care the relationship between alveolar bone loss ( ABL ) and environmental/systemic conditions. Material & Methods The study population consisted of subjects from the Purbasari tea estate on West Java, Indonesia. A full set of dental radiographs was obtained of each subject and amount of ABL was assessed. In addition, the following parameters were evaluated: plasma vitamin C, vitamin D 3 , HbA1c and CRP , the haptoglobin phenotype, presence of putative periodontopathic bacteria and viruses, dietary habits, smoking and anthropometrics. Results In this population 45% showed vitamin C depletion/deficiency, 82% had vitamin D 3 insufficiency/deficiency, 70% were in a pre‐diabetic state, 6% had untreated diabetes, 21% had elevated CRP values ranging from 3.1 to 16.1 mg/l. Results of the regression analysis, including all above mentioned parameters, showed four significant predictors, explaining 19.8% of the variance of ABL . Number of Porphyromonas gingivalis cells and CRP values showed a positive relationship with ABL , whereas BMI and number of guava fruit servings were negatively related. Conclusion Results confirm previous findings that elevated levels of P. gingivalis may be indicative for periodontitis progression. A new finding is that guava fruit consumption may play a protective role in periodontitis in a malnourished population.
Torres de Heens GL, Loos BG, van der Velden U. Monozygotic twins are discordant for chronic periodontitis: white blood Cell Counts and Cytokine production after ex vivo stimulation. J Clin Periodontol 2010; 37: 129–136. doi: 10.1111/j.1600‐051X.2009.01485.x . Abstract Objectives: The aim of this study was to investigate the extent of concordance in the number of leucocytes and their cytokine secretion after ex vivo stimulation in a twin population discordant for the amount of periodontal breakdown. Material and Methods: Venous blood was collected from 18 adult twin pairs (10 monozygotic and eight dizygotic twins). Each twin pair consisted of a diseased twin (proband) and his/her co‐twin. In venous blood, leucocytes were counted. The cytokines interleukin (IL)‐1 β , IL‐6, IL‐8, IL‐10 and IL‐12p40 were assessed after stimulation of monocytic cells, while IL‐13 and interferon (IFN)‐ γ were determined after lymphocytic stimulation. Results: In the study population as a whole, probands showed higher total numbers of leucocytes and lower IL‐12p40 levels compared with their co‐twins. In monozygotic twins, no difference was found in the leucocyte counts, but probands secreted more IL‐6 than their co‐twins; an opposite trend was found for IL‐12p40. Conclusion: The results suggest that the observed discordance in periodontal breakdown in the studied monozygotic twin population may be related to the relatively high levels of IL‐6 and the low levels of IL‐12p40 secretion after ex vivo stimulation of whole‐blood cell cultures. This cytokine secretion profile may be regarded as a risk indicator of periodontitis.
In spite of the remarkable success of current preventive efforts, periodontitis remains one of the most prevalent diseases of mankind. The objective of this workshop was to review critical scientific evidence and develop recommendations to improve: (i) plaque control at the individual and population level (oral hygiene), (ii) control of risk factors, and (iii) delivery of preventive professional interventions.Discussions were informed by four systematic reviews covering aspects of professional mechanical plaque control, behavioural change interventions to improve self-performed oral hygiene and to control risk factors, and assessment of the risk profile of the individual patient. Recommendations were developed and graded using a modification of the GRADE system using evidence from the systematic reviews and expert opinion.Key messages included: (i) an appropriate periodontal diagnosis is needed before submission of individuals to professional preventive measures and determines the selection of the type of preventive care; (ii) preventive measures are not sufficient for treatment of periodontitis; (iii) repeated and individualized oral hygiene instruction and professional mechanical plaque (and calculus) removal are important components of preventive programs; (iv) behavioural interventions to improve individual oral hygiene need to set specific Goals, incorporate Planning and Self monitoring (GPS approach); (v) brief interventions for risk factor control are key components of primary and secondary periodontal prevention; (vi) the Ask, Advise, Refer (AAR) approach is the minimum standard to be used in dental settings for all subjects consuming tobacco; (vii) validated periodontal risk assessment tools stratify patients in terms of risk of disease progression and tooth loss.Consensus was reached on specific recommendations for the public, individual dental patients and oral health care professionals with regard to best action to improve efficacy of primary and secondary preventive measures. Some have implications for public health officials, payers and educators.
Abstract This review aims to critically analyze the pathways of interaction and the pathogenic mechanisms linking periodontitis and oral bacteria with the initiation/progression of cancer at different body compartments. A higher risk of head and neck cancer has been consistently associated with periodontitis. This relationship has been explained by the local promotion of dysbiosis, chronic inflammation, immune evasion, and direct (epi)genetic damage to epithelial cells by periodontal pathobionts and their toxins. Epidemiological reports have also studied a possible link between periodontitis and the incidence of other malignancies at distant sites, such as lung, breast, prostate, and digestive tract cancers. Mechanistically, different pathways have been involved, including the induction of a chronic systemic inflammatory state and the spreading of oral pathobionts with carcinogenic potential. Indeed, periodontitis may promote low‐grade systemic inflammation and phenotypic changes in the mononuclear cells, leading to the release of free radicals and cytokines, as well as extracellular matrix degradation, which are all mechanisms involved in carcinogenic and metastatic processes. Moreover, the transient hematogenous spill out or micro‐aspiration/swallowing of periodontal bacteria and their virulence factors (i.e., lipopolysaccharides, fimbriae), may lead to non‐indigenous bacterial colonization of multiple microenvironments. These events may in turn replenish the tumor‐associated microbiome and thus influence the molecular hallmarks of cancer. Particularly, specific strains of oral pathobionts (e.g., Porphyromonas gingivalis and Fusobacterium nucleatum ) may translocate through the hematogenous and enteral routes, being implicated in esophageal, gastric, pancreatic, and colorectal tumorigenesis through the modulation of the gastrointestinal antitumor immune system (i.e., tumor‐infiltrating T cells) and the increased expression of pro‐inflammatory/oncogenic genes. Ultimately, the potential influence of common risk factors, relevant comorbidities, and upstream drivers, such as gerovulnerability to multiple diseases, in explaining the relationship cannot be disregarded. The evidence analyzed here emphasizes the possible relevance of periodontitis in cancer initiation/progression and stimulates future research endeavors.
Periodontitis is a complex, multifactorial disease and the susceptibility is genetically determined. In the last decade a multitude of research projects on genotyping of patients and controls in search of putative genetic risk factors has been performed. The disease (phenotype) however is also dependent on the presence of environmental and lifestyle factors, and their interaction with the various genes. Many candidate genes have been proposed and studied in relation to periodontitis. Most of the studied candidate genes code for proteins that play a role in the innate immune system. Some variants of candidate genes (gene polymorphisms) in the IL1 gene cluster and the FcgammaR genes are possibly associated with periodontitis. However till today there is no strong evidence for target genes and gene polymorphisms that play a key role in the susceptibility to and severity of periodontitis. Therefore genetic testing for periodontitis is currently not indicated.
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