## 1 Introduction  
Obstructive sleep apnea (OSA) is characterized by various and recurring episodes of reduction (hypopnea) or cessation (apnea) of the airflow during sleep. It results from the obstruction due to the collapse of the upper airway [1]. The pathophysiology of OSA is multifactorial and includes a reduction in upper airway dimensions that is caused by both anatomical and functional alterations (obesity or maxillofacial structural changes) and increased pharyngeal collapsibility due to reduced neuromuscular compensation and lack of the pharyngeal protective reflex during sleep [2; 3; 4; 5; 6]. OSA is one of the most prevalent chronic respiratory disorders. In recent population-based studies, the estimated prevalence of moderate to severe sleep-disordered breathing ranges from 3% to nearly 50% depending on the age group and sex. Recent studies suggest an increase in the incidence that is probably related to the growing prevalence of overweight and obese individuals [7; 8]. Extensive population-based studies have shown that untreated moderate or severe OSA is associated with severe complications. The most important are the increased cardiovascular and cerebrovascular disease, stroke, chronic inflammation, hypertension, and metabolic syndrome resulting in increased morbidity and mortality. The main symptoms are snoring, day sleepiness, noturia, frequent nocturnal waking caused by choking or gasping sensations, psychological or cognitive dysfunction, morning headaches, low concentration, irritability, and erectile dysfunction. Many patients report a reduction in their life quality due to obstructive sleep apnea [9; 10; 11; 12; 13]. OSA is an under-estimated problem even though there are many screening tools such as the STOP-BANG questionnaire, Epworth scale, and Berlin questionnaire [14; 15; 16; 17]. The gold standard for the diagnosis of OSA is polysomnography (level I study), which consists of an instrumental examination carried out in dedicated structures. Polysomnography involves the collection of seven or more data channels, including respiratory, electrocardiogram, electroencephalogram, and electrooculogram for sleep staging and electromyogram. Another solution for the diagnosis is the home-based polygraphy [18; 19; 20]. CPAP (continuous positive airway pressure) is the gold standard treatment for severe OSA, but since the 1980s, even mandibular advancement devices (MADs) were used as a therapy for OSA. MADs are widely used for mild and moderate OSA treatment, and several studies have demonstrated their effectiveness even in the treatment of severe OSA [21; 22]. MADs present higher compliance and are more convenient for the patient than CPAP [23; 24; 25; 26; 27]. Although mandibular advancement devices represent the gold standard in the treatment of mild and moderate OSA, they cause skeletal and dental modifications due to their use [28]. MADs are responsible for a small but statistically significant change in the dentition of long-term wearers. Skeletal changes are generally secondary to dental changes. Major dental modifications feature the tendency towards a reduction of overbite and overjet, maxillary incisors palatal tipping and mandibular incisor labial tipping. A moderate linkage exists between the length of treatment time (how long the device is worn), and the number of dental changes experienced [29]. Even if the modifications are not significant compared to the benefits that the use of the MAD brings, it is crucial to evaluate the periodontal consequences of these devices. Periodontal health is defined to be a state free from inflammatory periodontal disease. This situation, in turn, means that absence of inflammation associated with gingviitis or periodontitis [30]. An analysis of the literature reveals an epidemiological picture of the uneven periodontal disease with methodological discrepancies that make it difficult to compare the prevalence and severity of data [31].