In this pilot observational study, we found that obese and nonobese OSAS patients have different craniofacial morphologies that are correlated with the AHI and are associated with severe OSAS. In addition, although obese OSAS patients were characterized by a different equilibrium as assessed by a stabilometric assessment, we could not find any correlation or association with the severity of OSAS.
Research on cephalometric predictors in patients with OSAS is a cornerstone of sleep medicine [37–38], as is the investigation of early predictive factors such as craniofacial morphology in children [39]. In OSAS, upper airway obstruction can originate from various sources, including soft tissue collapse, such as the soft palate, or alterations in the position or dimensions of structures such as the tongue, maxilla, or mandible [40–43]. Upper airway obstruction can lead also to intermittent hypoxia, that has systemic effects in OSAS individuals [44]. The evaluation of craniofacial soft tissue is also crucial. For instance, Lee et al. reported that OSAS patients often exhibit broader and flatter mid- and lower-thirds of the face, accompanied by reduced maxillary and mandibular lengths [45]. Similarly, Tyan et al. identified significant correlations between craniofacial measurements and the severity of OSAS [46].
Our findings are in line with previous data reported by other studies. The evidence that OSAS patients are characterized by a different craniofacial morphology has also been described by Akpinar et al.; these authors reported that nonobese OSAS patients have smaller posterior airway spaces and different craniofacial morphologies than do habitual snorers (non-OSAS) and controls [19]. In fact, OSAS patients are characterized by mandibular micrognathias and retrognathia [47] and the retroposition of the maxilla and mandible [48–50]. OSAS are also characterized by a reduction in the posterior airway space or a multilevel obstruction of the airways [51–52]. Indeed, systematic reviews have recently reported that a reduced pharyngeal airway space and inferiorly placed hyoid bone are the cephalometric parameters most strongly associated with the severity of OSAS [53–54].
We herein reported that in nonobese OSAS patients, cephalometric measures were moderately correlated with the severity of OSAS; in addition, both the Sor-ANS and Sor-Me distances were associated with severe OSAS in nonobese patients, whereas only the Sor-ANS distance was associated with OSAS severity in obese patients. These findings may be explained by different underlying mechanisms in that subpopulation of patients. In fact, it may be postulated that in subjects with a BMI < 30 kg/m2, the severity of OSAS is mainly linked to alterations in skull facial dynamics. In these subjects, obesity likely plays a marginal role in the etiopathogenesis of the disease. Conversely, individuals with first-degree obesity develop OSAS for reasons binding mainly to obesity, which predisposes them to alveolar hypoventilation and airway collapse during sleep. In support of this hypothesis, Tangugsorn et al. also assessed differences in the cervicocraniofacial skeleton between obese and nonobese OSAS patients [55]. Researchers have found that among nonobese individuals with OSAS, anatomical irregularities are primarily limited to the skeletal structures of the cervical and craniofacial regions. In contrast, obese OSAS patients exhibit greater abnormalities in the soft tissue morphology of the upper airway, head posture, and position of the hyoid bone [55]. We also reported a certain correlation between the cephalometric assessment and the AHI (see Table 2).
Patients with OSAS exhibit sleep fragmentation and deprivation, which are suggested to be underlying factors contributing to impairments across various systems, including motor coordination [56–58]. The equilibrium is upheld through the ongoing and efficient integration of vestibular, visual, and proprioceptive inputs within the central nervous system [59]. These sensory data are consolidated and processed in the cerebellum, facilitating the stabilization and upkeep of the body's center of gravity through coordinated postural muscle contractions [60]. In this regard, OSAS patients were shown to be affected by a significant impairment in the vestibulo-ocular and sacculocollic reflexes and posturographic parameters [60–62]. It has also been suggested that these alterations may result from a chronic hypoxemic state that leads to a progressive reduction in vestibular function, generating disequilibrium [62–63]. Consistent with a previous study [22], we observed an increase in the area and velocity variance with eyes closed and teeth in contact, whereas the area was reduced under conditions with eyes open and teeth in contact, indicating strong muscle rigidity and a continuous search for the center of gravity, supported by the abnormal increase in the length of the trace (the number of oscillations the subject makes to find the center of gravity). Interestingly, it has also been demonstrated that daytime postural stability is influenced by and associated with nocturnal breathing disorders [56]. In our investigation, however, we found neither a correlation between postural disorders and the AHI nor an association between measurements from stabilometric examination and the presence of severe OSAS.
Our study has several limitations. First, given the study aim, we were unable to compute a precise sample size. Although other studies have recruited larger numbers of patients than ours [48], here, we report the findings of a pilot observational study with a total sample (40 patients) similar to other studies [49–50] or to their OSAS subpopulation [19]. In addition, we conducted nonparametric statistical analysis to be more conservative in the results [64]. Second, our findings may contrast with some literature data; this may also be due to an underpowered sample of patients. Third, given the observational nature of the study, the investigation may be affected by selection bias, and the findings may not be representative of a broader population; in addition, there could be several confounding variables [65]. This bias is dampened in our study by the enrollment of all consecutive OSAS patients, with no patients refusing to participate.