Association among Oral Health,Apical Periodontitis,CD14 Polymorphisms,and Coronary Heart Disease in Middle-aged Adults

Introduction

There is evidence to suggest that an association exists between oral infections and coronary heart disease (CHD). Subjects presenting lesions of endodontic origin (LEOs) or pulpal inflammation had an increased risk of developing CHD. However, findings concerning systemic manifestations of apical periodontitis (AP) remain controversial. An association between CD14 gene polymorphisms and atherosclerosis-associated diseases has been shown, but there are no data regarding an association between CD14 polymorphism and AP. This study evaluated associations between clinical oral health status, CD14 polymorphisms, and CHD.

Methods

A case-controlled clinical trial was designed to compare middle-aged adults with acute myocardial infarction or unstable angina (n = 51) within 12 months of the acute event defined as first manifestation with healthy controls (n = 49). Participants were matched for age, sex, and socioeconomic status. Indicators of oral disease and compliance were evaluated. CD14 polymorphisms were analyzed by restriction fragment length polymorphism–polymerase chain reaction.

Results

CHD subjects had a higher prevalence of oral diseases and lower compliance to oral preventive strategies than healthy controls. Multivariate analysis showed a positive association between missing teeth (odds ratio [OR] = 1.37; 95% confidence interval [CI], 1.02–1.85), the number of LEOs (OR = 4.37; 95% CI, 1.69–11.28), chronic periodontitis (OR = 5.87; 95% CI, 1.17–29.4), and CHD. No statistically significant association emerged between the CD14 C(−260)T and the CD14 C(−159)T polymorphism, endodontic or periodontal disease, and CHD.

Conclusions

Chronic oral diseases may increase the risk of CHD and may be an unconventional risk factor for CHD.     

Poly(ethylene glycol) hydrogels formed by thiol-ene photopolymerization for enzyme-responsive protein delivery

Degradable hydrogels have been extensively used in biomedical applications such as drug delivery, and recent interest has grown in hydrogels that degrade in recognition of a cellular response. This contribution describes a poly(ethylene glycol) (PEG) hydrogel platform with human neutrophil elastase (HNE) sensitive peptide cross-links formed using thiol-ene photopolymerization rendering the gel degradable at sites of inflammation. Further, protein therapeutics can be physically entrapped within the network and selectively released upon exposure to HNE. HNE-responsive hydrogels exhibited surface erosion where the degradation kinetics was influenced by changes in peptide k_cat, concentration of HNE, and concentration of peptide within the gel. Using this platform, we were able to achieve controlled, zero-order release of bovine serum albumin (BSA) in the presence of HNE, and release was arrested in the absence of HNE. To further exploit the advantages of surface eroding delivery systems, a smaller protein (carbonic anhydrase) was delivered at the same rate as BSA and only dependent on gel formulation and environmental conditions. Also, protein release was predicted from a 3-layered hydrogel device using mass loss data. Lastly, the bioactivity of lysozyme was maintained above 90% following the exposure to thiol-ene photopolymerization conditions.     

Patients' self-assessment of oral malodour and its relationship with organoleptic scores and oral conditions

Abstract: Objectives: The aim of this study was to compare patients’ self‐rating of oral malodour with organoleptic evaluation and to relate them to oral conditions. Methods: One hundred and eighty systemically healthy patients with a primary complaint of oral malodour participated in this cross‐sectional study. They were asked to complete a questionnaire regarding family and social discomfort and type of halitosis complaint, and to score the degree of their own oral malodour. The quality of the mouth air was assessed organoleptically by a calibrated odour judge. Odour‐judge scores and self‐assessments of bad breath were compared with one another as well as with clinical parameters (plaque index, bleeding index, probing depth and tongue coating score). Results: The organoleptic test revealed that 93.9% of the subjects were found actually to have halitosis. The self‐rating of oral malodour varied widely among patients. In 37.8% of patients, there was a correspondence between subjective and organoleptic measurements. The better correspondence was evident at 2–3 scores. The organoleptic ratings were significantly related to clinical parameters, whereas patients’ self‐measurements did not. The bleeding index had the highest correlation coefficient among the periodontal parameters examined (r = 0.665, P < 0.001). Conclusions: Self‐estimation of bad breath correlated well with the presence of oral malodour as determined by organoleptic examination. Patients with slight or moderate oral halitosis presented the highest correlation rate between self‐ and odour‐judge assessment.     

Gene--gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

Aggressive periodontitis (AgP) is a multifactorial disease. The distinctive aspect of periodontitis is that this disease must deal with a large number of genes interacting with one another and forming complex networks. Thus, it is reasonable to expect that gene-gene interaction may have a crucial role. Therefore, we carried out a pilot case-control study to identify the association of candidate epistatic interactions between genetic risk factors and susceptibility to AgP, by using both conventional parametric analyses and a higher order interactions model, based on the nonparametric Multifactor Dimensionality Reduction algorithm. We analyzed 122 AgP patients and 246 appropriate periodontally healthy individuals, and genotyped 28 polymorphisms, located within 14 candidate genes, chosen among the principal genetic variants pointed out from literature and having a role in inflammation and immunity. Our analyses provided significant evidence for gene--gene interactions in the development of AgP, in particular, present results: (a) indicate a possible role of two new polymorphisms, within SEPS1 and TNFRSF1B genes, in determining host individual susceptibility to AgP; (b) confirm the potential association between of IL-6 and Fc γ- receptor polymorphisms and the disease; (c) exclude an essential contribution of IL-1 cluster gene polymorphisms to AgP in our Caucasian-Italian population.     

Non-surgical periodontal treatment of cyclosporin A-induced gingival overgrowth: immunohistochemical results

Aim:  The present study was planned to analyze the effects of a 12-month non-surgical periodontal treatment on histologic and immunohistochemical features of cyclosporin A (CsA)-induced gingival overgrowth (GO).
Materials and methods:  Gingival samples were collected from 21 liver transplant subjects exhibiting CsA-induced GO prior to, and 12 months after non-surgical periodontal therapy including oral hygiene instructions, scaling and 2-month recall appointments, and also from 18 healthy control subjects. Gingival biopsy specimens were stained with hematoxylin–eosin and monoclonal antibodies for vimentin, CD3 (T-lymphocytes), CD20 (B-lymphocytes), CD34 (endothelium) and Ki-67 (fibroblasts proliferation rate), using a streptavidin-biotin-peroxidase complex method.
Results:  Total inflammatory cells, gingival vessels and fibroblast proliferation rate demonstrated significant reduction after non-surgical periodontal treatment ( P  < 0.0001) in overgrown gingiva, while B- and T-lymphocytes remained nearly unchanged ( P  = 0.61 and 0.33, respectively). At the 12-month evaluation no significant differences were found when comparing the gingival biopsies from CsA-treated patients and those from healthy controls ( P  > 0.05).
Conclusions:  Control of clinical inflammation by means of non-surgical periodontal treatment results both in lowering of inflammatory infiltrate and in changes in connective tissue composition. Thus, plaque-induced inflammation would seem to modulate the drug-gingival tissue interaction.
Clinical relevance:  A strict plaque control program play a pivotal role in the management of transplant patients exhibiting cyclosporin A-GO.