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Background: A variety of systemic diseases and conditions can affect the course of periodontitis or have a negative impact on the periodontal attachment apparatus. Gingival recessions are highly prevalent and often associated with hypersensitivity, the development of caries and non‐carious cervical lesions on the exposed root surface and impaired esthetics. Occlusal forces can result in injury of teeth and periodontal attachment apparatus. Several developmental or acquired conditions associated with teeth or prostheses may predispose to diseases of the periodontium. The aim of this working group was to review and update the 1999 classification with regard to these diseases and conditions, and to develop case definitions and diagnostic considerations. Methods: Discussions were informed by four reviews on 1) periodontal manifestions of systemic diseases and conditions; 2) mucogingival conditions around natural teeth; 3) traumatic occlusal forces and occlusal trauma; and 4) dental prostheses and tooth related factors. This consensus report is based on the results of these reviews and on expert opinion of the participants. Results: Key findings included the following: 1) there are mainly rare systemic conditions (such as Papillon‐Lefevre Syndrome, leucocyte adhesion deficiency, and others) with a major effect on the course of periodontitis and more common conditions (such as diabetes mellitus) with variable effects, as well as conditions affecting the periodontal apparatus independently of dental plaque biofilm‐induced inflammation (such as neoplastic diseases); 2) diabetes‐associated periodontitis should not be regarded as a distinct diagnosis, but diabetes should be recognized as an important modifying factor and included in a clinical diagnosis of periodontitis as a descriptor; 3) likewise, tobacco smoking – now considered a dependence to nicotine and a chronic relapsing medical disorder with major adverse effects on the periodontal supporting tissues – is an important modifier to be included in a clinical diagnosis of periodontitis as a descriptor; 4) the importance of the gingival phenotype, encompassing gingival thickness and width in the context of mucogingival conditions, is recognized and a novel classification for gingival recessions is introduced; 5) there is no evidence that traumatic occlusal forces lead to periodontal attachment loss, non‐carious cervical lesions, or gingival recessions; 6) traumatic occlusal forces lead to adaptive mobility in teeth with normal support, whereas they lead to progressive mobility in teeth with reduced support, usually requiring splinting; 7) the term biologic width is replaced by supracrestal tissue attachment consisting of junctional epithelium and supracrestal connective tissue; 8) infringement of restorative margins within the supracrestal connective tissue attachment is associated with inflammation and/or loss of periodontal supporting tissue. However, it is not evident whether the negative effects on the periodontium are caused by dental plaque biofilm, trauma, toxicity of dental materials or a combination of these factors; 9) tooth anatomical factors are related to dental plaque biofilm‐induced gingival inflammation and loss of periodontal supporting tissues. Conclusion: An updated classification of the periodontal manifestations and conditions affecting the course of periodontitis and the periodontal attachment apparatus, as well as of developmental and acquired conditions, is introduced. Case definitions and diagnostic considerations are also presented. [ABSTRACT FROM AUTHOR]

Multiple studies over many decades have demonstrated that diabetes mellitus and periodontitis are closely linked and may amplify one another. This review provides a different look at the complex association between these two common, chronic conditions and discusses decision-making in the management of affected individuals. [ABSTRACT FROM AUTHOR]

Aim To assess the periodontal status and number of missing teeth in patients with newly identified pre-diabetes or diabetes mellitus. Methods A total of 1097 subjects with previously undiagnosed diabetes were available for study, and were categorized into normoglycaemic, potentially pre-diabetes or potentially diabetes groups based on a point-of-care ( POC) HbA1c test. Results In fully adjusted models, significant differences were observed between all groups for the per cent of teeth with at least one site with a probing depth of ≥5 mm. For bleeding on probing, there were significant differences between diabetes and pre-diabetes ( p = 0.001), and between diabetes and normoglycaemic groups ( p = 0.002). For missing teeth, there were significant differences between the pre-diabetes and normoglycaemic groups ( p = 0.034), and the diabetes and normoglycaemic groups ( p = 0.004). Conclusions Individuals with previously unidentified pre-diabetes demonstrate a level of periodontal destruction between that observed for normoglycaemic individuals and persons with diabetes. These data emphasize the association of oral findings to dysglycaemia, and suggest that periodontal disease and tooth loss can be early complications of diabetes mellitus. [ABSTRACT FROM AUTHOR]

Aims: To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Methods: Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Results: Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small‐scale clinical studies and experiments in animal models suggest that IL‐1b, TNF‐a, IL‐6, OPG and RANKL may mediate periodontitis in diabetes. The AGE‐RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetesassociated periodontitis. A role for locally activated pro‐inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. Conclusion: There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro. [ABSTRACT FROM AUTHOR]

'Diabetes and Oral Disease: Implications for Health Professionals' was a one-day conference convened by the Columbia University College of Dental Medicine, the Columbia University College of Physicians and Surgeons, and the New York Academy of Sciences on May 4, 2011 in New York City. The program included an examination of the bidirectional relationship between oral disease and diabetes and the interprofessional working relationships for the care of people who have diabetes. The overall goal of the conference was to promote discussion among the healthcare professions who treat people with diabetes, encourage improved communication and collaboration among them, and, ultimately, improve patient management of the oral and overall effects of diabetes. Attracting over 150 members of the medical and dental professions from eight different countries, the conference included speakers from academia and government and was divided into four sessions. This report summarizes the scientific presentations of the event. a [ABSTRACT FROM AUTHOR]

Background: There is growing evidence that periodontal disease may be a source of systemic inflammation that impacts overall health. As such, periodontal disease is associated with an increased risk of systemic illnesses such as cardiovascular disease and adverse outcomes in diabetes mellitus and pregnancy. With the aim of assessing oral health knowledge and orientations of physicians in training, we surveyed incoming internal medicine trainees about their general knowledge, attitudes, and behaviors/practices about periodontal health and disease. Methods: A 16-question survey was distributed during orientation to incoming internal medicine trainees at a single urban teaching hospital in New York City in 2007 and 2008. Questions aimed to assess the knowledge levels of the subjects about periodontal disease and their attitudes toward discussing/evaluating the periodontal status of their patients. The study was approved by the Montefiore Institutional Review Board. Results: Of 125 incoming medical trainees queried, 115 responded (92% response rate). Of the 115 responders, 96% were medical interns. The median age of the trainees was 27 years (interquartile range: 26 to 29 years), and 61% were female. Overall, 34% of the trainees answered all five true/false general knowledge questions correctly, 82% reported that they never asked patients if they were diagnosed with periodontal disease, 90% reported not receiving any training about periodontal disease during medical school, 69% reported that they were not comfortable at all performing a simple periodontal examination, 17% agreed that patients expect physicians to discuss/screen for periodontal disease, 46% felt that discussing/evaluating the periodontal status of their patients was peripheral to their role as physicians, 76% reported never screening patients for periodontal disease, and 23% stated that they never referred patients to dentists. Conclusions: In this study, incoming internal medicine trainees had inadequate knowledge regarding periodontal disease. They were also generally uncomfortable with performing a simple periodontal examination. Oral health training in medical school and the medical postgraduate setting is recommended. [ABSTRACT FROM AUTHOR]

The author reflects on periodontal infections and diabetes mellitus in the U.S. She states that the puzzle of the periodontal infections-diabetes relationship is large, and due to the multi-factorial, complex aetiopathogenesis of both disease entities involved, it is a difficult one to solve. More, better-informed, coordinated and focused effort is necessary in order to add the many missing pieces and hopefully make some difference in the lives of those affected.

Aim: The association between diabetes mellitus and periodontal attachment and bone loss is well established. Most of the prior literature has focused on adults, and studies in children have mostly reported gingival changes. Our aim was to assess the periodontal status of a large cohort of children and adolescents with diabetes. Material and Methods: We examined 350 children with diabetes (cases) and 350 non-diabetic controls (6–18 years of age). Using three different case definitions for periodontal disease, which incorporated gingival bleeding and/or attachment loss findings, multiple logistic regression analyses adjusting for age, gender, ethnicity, frequency of prior dental visits, dental plaque, and examiner were performed. Results: Subjects with diabetes had increased gingival inflammation and attachment loss compared with controls. Regression analyses revealed statistically significant differences in periodontal destruction between cases and controls across all disease definitions tested (odds ratios ranging from 1.84 to 3.72). The effect of diabetes on periodontal destruction remained significant when we separately analysed 6–11 and 12–18 year old subgroups. Conclusions: These findings demonstrate an association between diabetes and an increased risk for periodontal destruction even very early in life, and suggest that programmes to address periodontal needs should be the standard of care for diabetic youth. [ABSTRACT FROM AUTHOR]

Objectives: We investigated the levels of subgingival plaque bacteria and serum IgG responses in patients with type 1 diabetes and non-diabetic controls of comparable periodontal status. Material and Methods: Fifty type 1 diabetes patients (mean duration 20.3 years, range 6–41) were age-and gender-matched with 50 non-diabetic individuals with similar levels of periodontal disease. Full-mouth clinical periodontal status was recorded, and eight plaque samples/person were collected and analysed by checkerboard hybridization with respect to 12 species. Homologous serum IgG titres were assessed by checkerboard immunoblotting. In a sub-sample of pairs, serum cytokines and selected markers of cardiovascular risk were assessed using multiplex technology. Results: Among the investigated species, only levels of Eubacterium nodatum were found to be higher in diabetic patients, while none of the IgG titres differed between the groups, both before and after adjustments for microbial load. Patients with diabetes had significantly higher serum levels of soluble E-selectin ( p=0.04), vascular cell adhesion molecule-1 (VCAM-1; p=0.0008), adiponectin ( p=0.01) and lower levels of plasminogen activator inhibitor-1 (PAI-1; p=0.02). Conclusions: After controlling for the severity of periodontal disease, patients with type 1 diabetes and non-diabetic controls showed comparable subgingival infection patterns and serum antibody responses. [ABSTRACT FROM AUTHOR]

OBJECTIVE -- To evaluate the level of oral disease in children and adolescents with diabetes. RESEARCH DESIGN AND METHODS -- Dental caries and periodontal disease were clinically assessed in 182 children and adolescents (6-18 years of age) with diabetes and 160 nondiabetic control subjects. RESULTS -- There were no differences between case and control subjects with respect to dental caries. Children with diabetes had significantly higher plaque and gingival inflammation levels compared with control subjects. The number of teeth with evidence of attachment loss (the hallmark of periodontal disease) was significantly greater in children with diabetes (5.79 ± 5.34 vs. 1.53 ± 3.05 in control subjects, unadjusted P < 0.001). When controlling for age, sex, ethnicity, gingival bleeding, and frequency of dental visits, diabetes remained a highly significant correlate of periodontitis, especially in the 12- to 18-year-old subgroup. In the case group, BMI was significantly correlated with destruction of connective tissue attachment and bone, but duration of diabetes and mean HbA[sub 1c] were not. CONCLUSIONS -- Our findings suggest that periodontal destruction can start very early in life in diabetes and becomes more prominent as children become adolescents. Programs designed to promote periodontal disease prevention and treatment should be provided to young patients with diabetes. [ABSTRACT FROM AUTHOR]

Abstract: Porphyromonas gingivalis is an etiologic agent of periodontal disease in humans, which has been linked to an increased risk for atherosclerosis-related events. In this study, we examined the effect of P. gingivalis infection on human macrophages with respect to foam cell formation, the hallmark of early atherogenesis, and the potential of P. gingivalis to induce its uptake by these cells. Human monocyte-derived macrophages were incubated with low density lipoprotein and infected with P. gingivalis FDC381 or its fimbriae deficient mutant, DPG3. Consistent with a role for fimbriae in this process, strain 381 significantly increased foam cell formation as compared to DPG3. Recovery of viable P. gingivalis in antibiotic protection experiments was significantly higher for strain 381 than for DPG3. By transmission electron microscopy, the wild-type strain was shown to adhere to and enter THP-1 cells. These results suggest that properties of P. gingivalis which render it capable of adhering to/invading other cell types may also be operative in macrophages and play an important role in its atherogenic potential. [Copyright &y& Elsevier]

We hypothesized that one mechanism underlying advanced periodontal disease in diabetes may involve oxidant stress in the gingiva induced by the effects of Advanced Glycation Endproducts (AGEs), the irreversible products of non- enzymatic glycation and oxidation of proteins and lipids which accumulate in diabetic plasma and tissue. Infusion of AGE albumin, a prototypic ligand, into mice resulted in increased generation of thiobarbituric acid reactive substances (TBARS) compared with infusion of non-glycated albumin in the gingiva, as well as in the lung, kidney and brain. Pretreatment of the animals with the anti- oxidants probucol or N-acetylcysteine (NAC) prevented the generation of TBARS in the gingiva. Affinity-purified antibody to AGEs demonstrated increased immunoreactivity for AGEs in the vasculature and connective tissues of the gingiva in streptozotocin-induced diabetic mice compared to non-diabetic controls. Increased immunoreactivity for AGEs was also demonstrated in the gingiva of diabetic humans compared with non-diabetic individuals via immunohistochemistry and ELISA. Consistent with these data, immunohistochemistry for heme oxygenase-1, a marker of enhanced oxidant stress, was increased in the gingival vasculature of diabetic mice and humans compared with non-diabetic controls. These data suggest that AGEs present in diabetic gingiva may be associated with a state of enhanced oxidant stress, a potential mechanism for accelerated tissue injury. [ABSTRACT FROM AUTHOR]

Abstract: Objective: A link between periodontal infections and an increased risk for vascular disease has been demonstrated. Porphyromonas gingivalis, a major periodontal pathogen, localizes in human atherosclerotic plaques, accelerates atherosclerosis in animal models and modulates vascular cell function. The receptor for advanced glycation endproducts (RAGE) regulates vascular inflammation and atherogenesis. We hypothesized that RAGE is involved in P. gingivalis''s contribution to pro-atherogenic responses in vascular endothelial cells. Methods and results: Murine aortic endothelial cells (MAEC) were isolated from wild-type C57BL/6 or RAGE−/− mice and were infected with P. gingivalis strain 381. P. gingivalis 381 infection significantly enhanced expression of RAGE in wild-type MAEC. Levels of pro-atherogenic advanced glycation endproducts (AGEs) and monocyte chemoattractant protein 1 (MCP-1) were significantly increased in wild-type MAEC following P. gingivalis 381 infection, but were unaffected in MAEC from RAGE−/− mice or in MAEC infected with DPG3, a fimbriae-deficient mutant of P. gingivalis 381. Consistent with a role for oxidative stress and an AGE-dependent activation of RAGE in this setting, both antioxidant treatment and AGE blockade significantly suppressed RAGE gene expression and RAGE and MCP-1 protein levels in P. gingivalis 381-infected human aortic endothelial cells (HAEC). Conclusion: The present findings implicate for the first time the AGE-RAGE axis in the amplification of pro-atherogenic responses triggered by P. gingivalis in vascular endothelial cells. [Copyright &y& Elsevier]

Abstract: Background: As a link between periodontal infections and an increased risk for vascular disease has been demonstrated, we assessed the ability of the Gram-negative periodontal pathogen Porphyromonas gingivalis to modulate properties of endothelial cells linked to inflammation and proatherogenic pathways. Methods and results: Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis strain 381 or its non-invasive fimbriae-deficient mutant, DPG3, and incubated with U-937 monocytes, or Jurkat T cells. P. gingivalis-infected HAEC demonstrated significantly increased adhesion of immune cells compared to non-infected cells or those infected with DPG3. Heat-killed bacteria had no effect on mononuclear cell adhesion and P. gingivalis LPS had only a minimal effect. P. gingivalis infection significantly increased HAEC expression of VCAM-1, ICAM-1 and E-selectin, and enhanced production of IL-6, IL-8 and MCP-1. Conclusion: These data demonstrate that live invasive P. gingivalis 381 elicits a pro-atherogenic response in HAEC. [Copyright &y& Elsevier]