Assessment of Screening for Nasal Obstruction among Sleep Dentistry Outpatients with Obstructive Sleep Apnea.

Oral appliances (OA), a common treatment modality for obstructive sleep apnea (OSA), are not suitable for patients with nasal obstruction. Rhinomanometry, the gold standard technique to assess nasal airway resistance, is not readily available in sleep dentistry clinics. We demonstrate the use of a portable lightweight peak nasal inspiratory flow (PNIF) rate meter to objectively assess nasal airflow and utilized the Nasal Obstruction Symptom Evaluation (NOSE) scale to subjectively assess nasal obstruction in 97 patients with OSA and 105 healthy controls. We examined the correlations between the following variables between the groups: demographics, body mass index, PNIF, NOSE scale scores, apnea-hypopnea index (AHI), minimum SpO2 (SpO2min), Mallampati classification, and Epworth Sleepiness Scale (ESS) scores. Patients with OSA had significantly lower PNIF values and higher NOSE scores than controls. In the patient group, PNIF was not significantly correlated with AHI, SpO2min, Mallampati classification, or NOSE or ESS scores. Lower PNIF values and higher NOSE scores suggested impaired nasal airflow in the OSA group. As daytime PNIF measurement bears no relationship to AHI, this cannot be used alone in predicting the suitability of treatment for OSA with OA but can be used as an adjunct for making clinical decisions.

Lip muscle training improves obstructive sleep apnea and objective sleep: a case report.

The present study assessed the potential of lip muscle training for improving sleep. A patient with heavy snoring, daytime sleepiness and dry mouth underwent lip muscle training. Lip closure force LCFmax increased by 67.3% and LCFmin by 152% post-training. AHI decreased from 12.2 to 3.9 events/h by reducing hypopneic episodes. TST, sleep stage N3 and REM sleep increased, and WASO, sleep stage N1, and AI decreased. The patient switched from mouth to nose breathing during sleep and stopped snoring. Improved LCF, by moving the tongue into the anterior-superior oral cavity, may increase upper airway space and reduce the hypopnea index.

Proatherogenic effect of interleukin-18 is exerted with high-fat diet, but not with normal diet in spontaneously hyperlipidemic mice.

AIM: It has been considered that interleukin (IL)-18, a T helper 1(Th1) type cytokine, has a promoting effect on atherosclerosis development. A previous mouse study demonstrated that short-term exogenous IL-18 promoted atherosclerosis through a Th1 type immune response; however, the serum IL-18 may have increased greatly beyond its physiological range, and the effect of increased serum IL-18 on atherosclerosis development has not been investigated under different conditions of dietary fat content. The purpose of this study was to reveal the effect of increased serum IL-18 within its physiological fluctuations on atherosclerosis development under different conditions of dietary fat content. METHODS: Spontaneously hyperlipidemic (SHL) mice were systemically supplied with IL-18 for 10 weeks by means of an in vivo gene transfer system with a high-fat diet containing 0.15% cholesterol or a normal diet. RESULTS: Serum IL-18 steadily elevated within its physiological fluctuations. An atherosclerotic lesion area in the aortic root significantly increased with a high-fat diet. Systemic cytokine balance shifted to a Th1-dominant state, and IL-12 mRNA in the arterial wall significantly increased with a high-fat diet; however, these findings were not observed with a normal diet. CONCLUSIONS: It was suggested that the proatherogenic effect of IL-18 is physiologically exerted exclusively with a high-fat diet through Th1 type immune responses, but not with a normal diet.

Aggregatibacter actinomycetemcomitans accelerates atherosclerosis with an increase in atherogenic factors in spontaneously hyperlipidemic mice.

Cariogenic and periodontal pathogens are thought to be etiological factors in the development of cardiovascular disease. We assessed the involvement of the periodontal pathogen Aggregatibacter actinomycetemcomitans and cariogenic pathogen Streptococcus mutans in the development of atherosclerosis in apolipoprotein E-deficient spontaneously hyperlipidemic (Apoe(shl)) mice. The mice were treated intravenously with A. actinomycetemcomitans HK1651, S. mutans GS-5, or phosphate-buffered saline three times a week for 3 weeks and killed at 15 weeks of age. The areas of the aortic sinus that were covered with atherosclerotic plaque were significantly larger in Apoe(shl) mice challenged with A. actinomycetemcomitans compared with S. mutans- or vehicle-challenged mice. Aggregatibacter actinomycetemcomitans challenge increased serum high-sensitive C-reactive protein and lipopolysaccharide levels. Bacterial DNA was detected in the blood, heart, and spleen, but not in the liver. Furthermore, serum interleukin-6 (IL-6), IL-8, tumor necrosis factor alpha, and MCP-1 levels and Toll-like receptor (TLR)2, TLR4, ICAM-1, E-selectin, P-selectin, LOX-1, HSP60, CCL19, CCL21, CCR7, and MCP-1 expressions in the aorta were significantly increased in mice challenged with A. actinomycetemcomitans. These results suggest that systemic infection with A. actinomycetemcomitans accelerates atherosclerosis in Apoe(shl) mice by exposing the whole microorganisms or their products, followed by initiating inflammation. Increases in proatherogenic factors may explain the aggravation of atherosclerosis by A. actinomycetemcomitans infection.

Intranasal immunization with Porphyromonas gingivalis and atherosclerosis.

Periodontal disease is a highly prevalent disorder affecting up to 90% of the global population. Recent epidemiological studies have shown that an association exists between periodontal disease and cardiovascular disease. Porphyromonas gingivalis, the causative agent of destructive chronic inflammation in the periodontium, can accelerate atheroma deposition in animal models. Emerging evidence suggests that vaccination against this pathogen's virulence factors may confer disease resistance. In this review, we focus on the role of inflammatory mechanisms in the formation and activation of atherosclerotic plaques accelerated by P. gingivalis in an apo E-deficient mouse model. Further, we examine whether a nasal vaccine-induced antigen-specific mucosal response can reduce P. gingivalis-accelerated atherosclerosis.

Relation of secretory phospholipase A(2) and high-sensitivity C-reactive protein to Chlamydia pneumoniae infection in acute coronary syndromes.

BACKGROUND: Recently it has become clear that inflammatory changes play a part in the development of atherosclerosis, including coronary artery disease, and Chlamydia pneumoniae (C. pneumoniae) is thought to be a proinflammatory factor. The plasma concentration of high-sensitive C-reactive protein (hs-CRP) is a potential predictor of outcome in atherosclerotic diseases. Recent interest has focused on secretory group IIA phospholipase A(2) (sPLA (2)) in regard to the progression of atherosclerotic disease. METHODS AND RESULTS: The concentrations of sPLA(2), hs-CRP, and the titers of C. pneumoniae IgG and IgA antibodies were measured in blood samples. The study groups were an acute coronary syndrome (ACS) group, old myocardial infarction/angina pectoris (OMI/AP) group, and a control group. The concentrations of sPLA(2) and hs-CRP in the ACS group and the OMI/AP group were higher than in the control group. The titers of C. pneumoniae IgG and IgA were higher in the ACS group than in the control group. The sPLA(2) concentration was higher in those who were positive to C. pneumoniae IgG/IgA than in those who were negative. CONCLUSION: Increased concentrations of sPLA(2) reflect participation in the progression of coronary artery disease. The sPLA(2) concentration was higher in patients positive for C. pneumoniae than in those negative for C. pneumoniae, so C. pneumoniae infection poses a greater risk for ACS in those individuals than in those who are free of such infection.

Involvement of inflammation in acute coronary syndromes assessed by levels of high-sensitivity C-reactive protein, matrix metalloproteinase-9 and soluble vascular-cell adhesion molecule-1.

OBJECTIVES: Inflammation is important in the development of atherosclerosis. Matrix metalloproteinases (MMPs) and interferon-gamma which participate in collagen degradation are pathological factors in plaque vulnerability as an important mechanism underlying acute coronary syndrome. This study investigated whether inflammation is related to the onset of acute coronary syndrome. METHODS: This study included 56 patients with acute coronary syndrome (ACS group), 104 patients with chronic coronary artery disease (S group), and 38 control subjects with no evidence of ischemic heart disease (C group). High-sensitivity C-reactive protein (hs-CRP), MMP-9, and interferon-gamma were measured in peripheral blood samples. Soluble adhesion molecules (VCAM-1, ICAM-1) were also measured as inflammatory markers. RESULTS: The hs-CRP level was significantly higher in the ACS group (44.5 mg/l) than in the S group (2.1 mg/l) and the C group (0.6 mg/l) (p < 0.0001). The MMP-9 level was also significantly higher in the ACS group (333.8 ng/ml) than in the S group (110.8 ng/ml) and the C group (72.0 ng/ml) (p < 0.0001). The VCAM-1 level was significantly higher in the ACS group (506.5 ng/ml) than in the C group (448.8 ng/ml) (p < 0.05). The ICAM-1 level and the interferon-gamma level did not differ between the groups. There was a significant positive correlation between the level of hs-CRP and the level of the collagen degradation product MMP-9 (r = 0.52) in all subjects. CONCLUSIONS: These results suggest that plaque destabilized by MMP-9 produced in response to inflammation participates in the mechanism of acute coronary syndrome.

Inhibitory effect on arterial injury-induced neointimal formation by adoptive B-cell transfer in Rag-1 knockout mice.

We investigated the effect of B-cell reconstitution in immune-deficient Rag-1 knockout (KO) mice subjected to arterial injury. After 21 days, injury induced a 4- to 5-fold increase in neointimal formation in Rag-1 KO mice fed normal chow compared with wild-type (WT) mice (0.020+/-0.0160 [n=8] versus 0.0049+/-0.0022 [n=8] mm(2), respectively; P<0.05) and in western-type diet-fed Rag-1 KO mice compared with WT mice (0.0312+/-0.0174 [n=7] versus 0.0050+/-0.0028 [n=6] mm(2), respectively; P<0.05). To investigate the role of B cells in response to injury, Rag-1 KO mice were reconstituted with B cells derived from the spleens of WT mice, with donors and recipients on the same diet. Reconstitution of Rag-1 KO mice with B cells from WT mice (both fed normal chow) reduced neointimal formation compared with the effect in unreconstituted Rag-1 KO mice (0.0076+/-0.0039 [n=9] versus 0.020+/-0.0160 [n=8] mm(2), respectively; P<0.05). Reconstitution of Rag-1 KO mice with B cells from WT mice (both fed a western diet) reduced neointimal formation compared the effect in Rag-1 KO mice (0.0087+/-0.0037 [n=8] versus 0.0312+/-0.0174 [n=7] mm(2), respectively; P<0.05). Injured carotid arteries from reconstituted Rag-1 KO mice had detectable IgM and IgG, indicating viable transfer of B cells. The results suggest that B cells modulate the response to arterial injury.