Weak association between sleep bruxism and obstructive sleep apnea. A sleep laboratory study.

PURPOSE: No definitive associations or causal relationships have been determined between obstructive sleep apnea-hypopnea (OSAH) and sleep bruxism (SB). The purpose of this study was to investigate, in a population reporting awareness of both OSAH and SB, the associations between each specific breathing and jaw muscle event. METHODS: Polysomnography and audio-video data of 59 patients reporting concomitant OSAH and SB history were analyzed. Masseteric bursts after sleep onset were scored and classified into three categories: (1) sleep rhythmic masticatory muscle activity with SB (RMMA/SB), (2) sleep oromotor activity other than RMMA/SB (Sleep-OMA), and (3) wake oromotor activity after sleep onset (Wake-OMA). Spearman's rank correlation coefficient analyses were performed. Dependent variables were the number of RMMA/SB episodes, RMMA/SB bursts, Sleep-OMA, and Wake-OMA; independent variables were apnea-hypopnea index (AHI), arousal index(AI), body mass index(BMI), gender, and age. RESULTS: Although all subjects had a history of both SB and OSAH, sleep laboratory results confirmed that these conditions were concomitant in only 50.8 % of subjects. Moderate correlations were found in the following combinations (p < 0.05); RMMA/SB episode with AI, RMMA/SB burst with AI and age, Sleep-OMA burst with AHI, and Wake-OMA burst with BMI. CONCLUSIONS: The results suggest that (1) sleep arousals in patients with concomitant SB and OSAH are not strongly associated with onset of RMMA/SB and (2) apnea-hypopnea events appear to be related to higher occurrence of other types of sleep oromotor activity, and not SB activity. SB genesis and OSAH activity during sleep are probably influenced by different mechanisms.

Temporal association between sleep apnea-hypopnea and sleep bruxism events.

There is some evidence suggesting that obstructive sleep apnea-hypopnea syndrome is concomitant with sleep bruxism. The aim of this study was to investigate the temporal association between sleep apnea-hypopnea events and sleep bruxism events. In an open observational study, data were gathered from 10 male subjects with confirmed obstructive sleep apnea-hypopnea syndrome and concomitant sleep bruxism. Polysomnography and audio-video recordings were performed for 1 night in a sleep laboratory. Breathing, brain, heart and masticatory muscle activity signals were analysed to quantify sleep and sleep stage duration, and number and temporal distribution of apnea-hypopnea events and sleep bruxism events. Apnea-hypopnea events were collected within a 5-min time window before and after sleep bruxism events, with the sleep bruxism events as the pivotal reference point. Two temporal patterns were analysed: (i) the interval between apnea-hypopnea events termination and sleep bruxism events onset, called T1; and (ii) the interval between sleep bruxism events termination and apnea-hypopnea events onset, called T2. Of the intervals between sleep bruxism events and the nearest apnea-hypopnea event, 80.5% were scored within 5 min. Most intervals were distributed within a period of <30 s, with peak at 0-10 s. The T1 interval had a mean length of 33.4 s and was significantly shorter than the T2 interval (64.0 s; P < 0.05). Significantly more sleep bruxism events were scored in association with the T1 than the T2 pattern (P < 0.05). Thus, in patients with concomitant obstructive sleep apnea-hypopnea syndrome and sleep bruxism, most sleep bruxism events occurred after sleep apnea-hypopnea events, suggesting that sleep bruxism events occurring close to sleep apnea-hypopnea events is a secondary form of sleep bruxism.

Effect of low-dose theophylline on airway inflammation in COPD.

OBJECTIVE: Recent studies have shown that theophylline may exert anti-inflammatory effects on neutrophils. We undertook to assess the effect of theophylline on airway inflammation in COPD. METHODOLOGY: We performed a 4-week randomized double-blind, placebo-controlled study in 11 theophylline-naive patients with mild to moderate COPD. After a 1-week run-in period, six subjects were administered 400 mg/day theophylline (Theodur; Nikken Chemicals Co. Ltd, Tokyo, Japan) for 4 weeks, while five subjects were administered a placebo. Induced sputum was obtained before and after the run-in period and then after 2 and 4 weeks of treatment. Cell differential count and levels of interleukin-8, matrix metalloproteinase-9, neutrophil elastase (NE), myeloperoxidase (MPO), alpha1-antitrypsin (alpha1-AT), leukotriene B4 and tissue inhibitor of metalloproteinases-1 (TIMP-1) were assessed. RESULTS: No variable was significantly different during the run-in period or with placebo treatment. In contrast, theophylline treatment significantly decreased NE and MPO levels at 4 weeks, although the cell differential count did not change appreciably as a result of treatment. CONCLUSION: These results suggest that 4 weeks of theophylline treatment attenuates neutrophil-associated inflammation in the airways of mild to moderate COPD patients. However, the clinical benefits remain to be determined.

Tissue hypoxia in sleep apnea syndrome assessed by uric acid and adenosine.

STUDY OBJECTIVE: Although the overnight increase in urinary uric acid/creatinine ratio (DeltaUA/Cr) is considered by some to be a marker of tissue hypoxia in patients with obstructive sleep apnea-hypopnea syndrome (OSAS), this index is not universally accepted. The purpose of this study was to confirm the validity of DeltaUA/Cr as a marker of tissue hypoxia by measuring the plasma level of adenosine during sleep, and also to test the hypothesis that the heart rate (HR) response to apnea is a determinant of tissue hypoxia. DESIGN: Intergroup comparative study. SETTING: A university hospital, Sapporo, Japan. PATIENTS: Eighteen patients with OSAS who had apnea-associated, moderate-to-severe arterial desaturation. The patients were classified into two groups: the DeltaUA/Cr-positive group, who were considered to have tissue hypoxia, and the DeltaUA/Cr-normal group, who were not. MEASUREMENTS AND RESULTS: Although there were no significant differences between two groups of the patients in either arterial desaturation parameters or the apnea-hypopnea index, the plasma level of adenosine during sleep was significantly higher in the DeltaUA/Cr-positive group than in the DeltaUA/Cr-normal group. Successful treatment with nasal continuous positive airway pressure significantly decreased both DeltaUA/Cr and the plasma level of adenosine only in the DeltaUA/Cr-positive group. The magnitude of the HR increase after the termination of apnea was significantly smaller in the DeltaUA/Cr-positive group. CONCLUSIONS: DeltaUA/Cr is a marker of tissue hypoxia, which does not necessarily parallel arterial desaturation indexes in OSAS. Intersubject variability in the HR response to apnea may explain the discrepancy between tissue hypoxia and arterial desaturation indexes.