Upper airway surface tension but not upper airway collapsibility is elevated in primary Sjögren's syndrome

Abstract

Study objectives: Primary Sjögren's syndrome is an autoimmune disease typified by xerostomia (dry mouth) that, in turn, could lead to increased saliva surface tension (gamma) and increased upper airway collapsibility. Fatigue, of unknown etiology, is also frequently reported by patients with primary Sjögren's syndrome. Recent preliminary data indicate a high prevalence of obstructive sleep apnea in healthy-weight women with primary Sjögren's syndrome. Concurrent research highlights a significant role of gamma in the maintenance of upper airway patency. The aim of this study was to compare oral mucosal wetness, saliva gamma, and upper airway collapsibility during wake and sleep between women with primary Sjögren's syndrome and matched control subjects.

Setting: Participants slept in a sound-insulated room with physiologic measurements controlled from an adjacent room.

Participants: Eleven women with primary Sjögren's syndrome and 8 age- and body mass index-matched control women.

Interventions: Upper airway collapsibility index (minimum choanal-epiglottic pressure expressed as a percentage of delivered choanal pressure) was determined from brief negative-pressure pulses delivered to the upper airway during early inspiration in wakefulness and sleep.

Measurements and results: Patients with primary Sjögren's syndrome had significantly higher saliva gamma ("pull-off" force method) compared with control subjects (67.2 +/- 1.1 mN/m versus 63.2 +/- 1.7 mN/m, P < 0.05). Upper airway collapsibility index significantly increased from wake to sleep (Stage 2 and slow wave sleep) but was not different between groups during wake (primary Sjögren's syndrome versus controls; 36.3% +/- 8.0% vs 46.0 +/- 13.8%), stage 2 sleep (53.1% +/- 11.9% vs 63.4% +/- 7.2%), or slow-wave sleep (60.8% +/- 12.2% vs 60.5% +/- 9.3%).

Conclusions: Despite having a significantly "stickier" upper airway, patients with primary Sjögren's syndrome do not appear to have abnormal upper airway collapsibility, at least as determined from upper airway collapsibility index.

Figure 1

Schematic of the respiratory circuit. Arrows indicate direction of airflow: black during normal breathing, grey during brief negative pressure pulses.

Figure 2

Comparison of gravimetric fluid absorption after 5-sec absorbent paper contact on the posterior midline of the tongue (μL/5 sec) in subjects with primary Sjögren's syndrome (n = 11) and control subjects without Sjögren's syndrome (n = 8) at evening, morning, and combined collection times. There were no significant differences between groups or across collection times. Values are mean ± SEM.

Figure 3

Saliva surface tension (mN/m) in subjects with primary Sjögren's syndrome and control subjects without Sjögren's syndrome. Patients with primary Sjögren's syndrome had significantly higher saliva surface tension than controls (*P < 0.05). Values are mean ± SEM. Primary Sjögren's syndrome evening, n = 7; primary Sjögren syndrome's morning, n = 8; controls at both collection times, n = 8.

Figure 4

Ensemble averaged choanal (Pcho) and epiglottic (Pepi) pressures during negative pressure pulses applied during wake (A, B) and stage 2 sleep (C, D) in patients with primary Sjögren's syndrome (B, D) and control subjects without Sjögren's syndrome (A, C). Raw data averaged from 500 msec before to 1,000 msec after the pulse. Values are mean ± SEM. Primary Sjögren's syndrome wake, n = 11; primary Sjögren's syndrome stage 2 sleep, n = 9; controls in both states, n = 8.

Figure 5

Comparison of collapsibility index, as a measure of upper airway collapsibility, between primary Sjögren's syndrome and non-primary Sjögren's syndrome controls during wake, stage 2 and SWS. Collapsibility index was calculated from ensemble averaged pulses for each state using the formula: minimum Pcho − Pepi pressure (at minimum Pcho)/ minimum Pcho; expressed as a percentage. *P < 0.05 compared to wake. Values are mean ± SEM. Primary Sjögren's syndrome wake, n = 11; primary Sjögren's syndrome stage 2 sleep, n = 9; primary Sjögren's syndrome slow-wave sleep (SWS), n = 7; controls wake and stage 2 sleep, n = 8; controls SWS, n = 7.