64 (47 M and 17 F; mean age: 50.3 ± 9.1 yrs in MAD group, 55.4 ± 9.8 yrs in nCPAP group, and 51.3 ± 10.1 yrs in placebo group); full polysomnographic recordings in the sleep laboratory of the Slotervaart Medical Centre, using Siesta hardware and Profusion software (Compumedics, Abbotsford, VIC, Australia) (5 ≥ e ≤ 45)
Customised and titratable device
6 ± 2 months
No differences in the AHI were found between the MAD and nCPAP therapy (), whereas the changes in AHI in the two therapy groups were significantly greater than those in the placebo group ( and , respectively)
72 (57 M and 15 F; mean age: 57 ± 8 yrs in active OA group and 59 ± 9 yrs in control OA group); ambulatory nocturnal somnographic registration (Embletta PDS device; Medcare Flaga, Iceland) (≥10)
Customised monobloc nontitratable device
3 months
Significant AHI reduction in patients with active OA (). Significant 24 h mean systolic blood pressure reduction was noted only in a subgroup of patients with ambulatory 24 h mean systolic BP > 135/85 mmHg and AHI >15
99 (70 M and 29 F; mean age: 47.3 ± 10.1 yrs in SPT group and 49.2 ± 10.2 yrs in OA group); a digital PSG system (Embla A10, Broomfield, CO, USA) (positional OSAS)
Customised and titratable device
3 months
There was no statistically significant difference in AHI reduction between the two groups
150 (14.4% were female; mean age: 54.8 ± 9.9 yrs in MAD group, 52.9 ± 10.5 yrs in sham device group); in-laboratory PSG (≥30)
Customised and titratable device
2 months
After adjustment for baseline values, age, sex, BMI, AHI, and smoking habits, the difference in RHI outcome between effective MAD and sham device was not statistically significant
Parallel RCT (other customised and titratable MAD)
103 (ST group mean age: 50.5 ± 10.9 yrs, 41 M, 10 F; TAP group mean age: 50.4 ± 11.1 yrs, 45 M, 7 F); polysomnography (PSG) (≤40)
Customised and titratable device
Median time interval of follow-up: 42.7 months for IST appliance; 41.5 months for TAP appliance
Significant reduction of AHI was noticed with both the devices. In the short-term evaluation, the device that held the mandible firmly in a protrusive position during the entire sleep (TAP), without allowing mouth opening, was significantly better than the other one (IST)
73 (59 M, 14 F; mean age: 48 ± 11); polysomnography (PSG) (≥10)
Customised and titratable device
1 month
Both MLST and ESS values were better at follow-up. A significant reduction of the following values in MAS group with respect to control group was noticed: AHI, snoring frequency, mean and maximum snoring intensity, arousal index, and MinSaO2
103 (92 M and 11 F); polysomnography (Embla® A10 digital recorder, Medcare, Reykjavík, Iceland) (≥5)
Customised and titratable device
3 months
Noninferiority of oral appliance therapy was considered to be established when the lower boundary of this interval exceeded −25%. The lower boundary of the confidence interval was −21.7%, indicating that oral appliance therapy was not inferior to CPAP for effective treatment of obstructive sleep apnoea. However, subgroup analysis revealed that oral appliance therapy was less effective in individuals with severe disease (apnoea-hypopnea index >30)
101 (79 M and 22 F); PSG (Alice 3 or Alice 4 Diagnostics System, Respironics, Atlanta, USA) (between 5 and 40)
Customised but not titratable device
2.5 months
Nadir O2 and AHI improved significantly with respect to baseline values both in CPAP group and in OA group. ESS significantly decreased in all three groups
91 (62 M and 29 F; mean age: 49.8 ± 10.6 yrs in OA group and 54.1.2 ± 9.4 yrs in placebo device group); polysomnographic sleep recordings (Embla, Natus Neurology) (<30)
Customised and titratable device
4 months
No significant difference for the primary outcomes (ESS, KSS, OSLER test, SF-36) between the two groups
126 (102 M and 24 F; mean age: 49.5 ± 11.2 yrs); polysomnography (PSG) (>10)
Customised and titratable device
1 month
MAD was noninferior to CPAP for control of 24MAP (mean CPAP-MAD difference (95% confidence interval), 0.2 (20.7 to 1.1) mm Hg). In the subgroup of patients who were initially hypertensive, there were consistent treatment-related 24-hour BP improvements of 2–4 mm Hg in all indexes with neither treatment having a superior effect
Crossover RCT, no treatment; thermoplastic “boil and bite” not titratable device (SleepPro 1); semi-bespoke not titratable device produced from a patient-moulded dental impression kit (SleepPro 2)
90 (72 M and 18 F; mean age: 50.9 ± 11.6 yrs); respiratory polysomnography (rPSG) (5≥ and ≤30)
Customised but not titratable bespoke MAD (bMAD)
1 month
All three MADs significantly decreased the AHI against no treatment by 26% (95% CI: 11% to 38%) for the SP1, 33% (95% CI: 24% to 41%) for the SP2, and 36% (95% CI: 24% to 45%) for the bMAD. A similar effect was found for all devices against no treatment for 4% oxygen desaturation index (4% ODI). The bMAD had a significant effect on minimum oxygen saturation compared with no treatment and the other devices
95 (mean age: 49, 3 yrs in OA group and 51 yrs in UPPP group); somnography (>25)
Customised monobloc nontitratable device
12 months
Significant reduction of AI, AHI, ODI, and SI in both groups at 6 and 12 months. After 12 months, OA gave better results than UPPP. Success rate for AI and AHI resolution with OA was, respectively, 95% and 81%. Success rate for AI and AHI resolution with UPPP was, respectively, 70% and 60%
